INSERT INTO `ChimerPub_dump` VALUES ('9431', 'NKG2A_CD94', '', 'NKG2A', 'CD94', '9842883', '10', '', '', '', '', '', '', '', '', '', 'Phosphoantigen activation induces surface translocation of intracellular CD94/NKG2A class I receptor on CD94- peripheral Vgamma9 Vdelta2 T cells but not on CD94- thymic or mature gammadelta T cell clones..     ///    In the present study we show that most CD94- Vgamma9Vdelta2 PBL ex vivo express an intracellular pool of CD94/NKG2-A receptors that is translocated to the cell surface upon activation by phosphoantigens or IL-2.     ///    Altogether these results provide new insights into the regulation of CD94/NKG2-A expression on T lymphocytes and suggest the existence of distinct mechanisms controlling in vivo and in vitro induction of IR on these cells..     ///    \"They also express various MHC class I-specific inhibitory receptors (IR), in particular CD94/ NKG2-A heterodimers, which participate in the fine tuning of their TCR-mediated activation threshold. \"    ///    \"In stark contrast, intracellular CD94/NKG2-A complexes are undetectable in CD94- thymus or PBL-derived mature Vdelta2 T cell clones, and no surface induction is observed following phosphoantigen activation of T cell clones. \"'), ('9432', 'REL_BCL11A', '', 'REL', 'BCL11A', '18940474', '10', 'Hodgkin lymphoma', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'To identify the translocation partners, these cases were further studied with probes for the MYC, BCL2, BCL6, BCL3, REL/BCL11A, JAK2/PDCD1LG2 (alias PDL2) C14orf43, and C2TA loci. '), ('9433', 'EML4_ALK', '', 'EML4', 'ALK', '20028651', '10', 'lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Personalized medicine is becoming a reality for patients with EGFR mutation as well as for the recruitment of patients in certain clinical trials (EML4-ALK translocation, KRAS mutation...). '), ('9434', 'RPL7_L12', '', 'RPL7', 'L12', '16337596', '10', '', '', '', '', '', '', '', '', '', 'Interaction of the G\' domain of elongation factor G and the C-terminal domain of ribosomal protein L7/L12 during translocation as revealed by cryo-EM..     ///    \"Molecular analyses of the cryo-EM maps show: (1) that three structural components, the N-terminal domain of ribosomal protein L11, the C-terminal domain of ribosomal protein L7/L12, and the G\' domain of EF-G, participate in formation of the ALC. \"    ///    and (2) that both EF-G and the ribosomal protein L7/L12 undergo large conformational changes to form the ALC.. '), ('9435', 'TR3_NUR77', '', 'TR3', 'NUR77', '15519684', '10', '', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'NUR77/TR3 was a nuclear protein before noise, but following noise translocated to the cytoplasm.     ///    \"The intense PTS noise induced several immediate early genes encoding both transcription factors (c-FOS, EGR1, NUR77/TR3) and cytokines (PC3/BTG2, LIF and IP10). \"    ///    \"Three proteins (EGR1, NUR77/TR3, and IP10) were detected in many regions of the unexposed cochlea. \"'), ('9436', 'SIAH1_GAPDH', '', 'SIAH1', 'GAPDH', '16391220', '10', '', '', '', '', '', '', '', '', '', 'Cytotoxic stimuli, via nitric oxide generation, lead to the binding of GAPDH to the protein Siah1, translocation of GAPDH-Siah1 to the nucleus, and ultimately cell death. '), ('9437', 'HLA-DQ_DP', '', 'HLA-DQ', 'DP', '9098404', '10', '', 'PCR', '', '', '', '', '', '', '', ' HLA-DR/DQ-DP linkage disequilibrium was investigated in healthy, unrelated British (n = 150) and French Canadian (n = 67) Caucasoid subjects.     ///    Absence of strong HLA-DR/DQ-DP linkage disequilibrium in the British and French Canadian Caucasoid populations.. '), ('9438', 'HLA-DR_DP', '', 'HLA-DR', 'DP', '9098404', '10', '', 'PCR', '', '', '', '', '', '', '', ' HLA-DR/DQ-DP linkage disequilibrium was investigated in healthy, unrelated British (n = 150) and French Canadian (n = 67) Caucasoid subjects.     ///    Absence of strong HLA-DR/DQ-DP linkage disequilibrium in the British and French Canadian Caucasoid populations.. '), ('9439', 'RET_PTC', '', 'RET', 'PTC', '19777762', '10', 'thyloid cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'This knowledge has in turn led to the development of a range of targeted therapies, some specific to thyroid cancer genetic alterations such as the RET/PTC translocation, and others that exploit general malignant properties such as angiogenesis. '), ('9440', 'ETO_AML1', '', 'ETO', 'AML1', '23612831', '10', 'acute myeloid leukemia', '', '', '', '', '', '', '', '', '[Acute myeloid leukemia (aml) subtype M2 with variation of the t (8;21)translocation and AML1/ETO expression].. '), ('9441', 'IL4RA_IL4', '', 'IL4RA', 'IL4', '16313681', '10', 'asthma', 'PCR', '', '', '', '', '', '', '', ' IL4/IL4RA pathway plays an important role in atopy and asthma. '), ('9442', 'MTOR_AKT1', '', 'MTOR', 'AKT1', '25537506', '10', 'hepatocellular carcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'In human HCC specimens, nuclear translocation of SKP2 was associated with activation of the AKT/mTOR and Ras/MAPK pathways, but not with ?-catenin mutation or activation.     ///    \"At the molecular level, preneoplastic and neoplastic liver lesions from SKP2/N-RasV12 and SKP2/myr-AKT1 mice exhibited a strong induction of AKT/mTOR and Ras/MAPK pathways. \"'), ('9443', 'APPL1_AMPK', '', 'APPL1', 'AMPK', '24255018', '10', '', '', '', '', '', '', '', '', '', 'In summary, these data are the first to report the adiponectin stimulated APPL1-AMPK signaling axis in cardiac fibroblasts and characterize MT1-MMP translocation, MMP2 activity and cell migration as functional outcomes.     ///    \"Adiponectin mediated APPL1-AMPK signaling induces cell migration, MMP activation, and collagen remodeling in cardiac fibroblasts.. \"'), ('9444', 'MAPK14_NFKB1', '', 'MAPK14', 'NFKB1', '12853969', '10', 'prostate cancer\r\r', '', 'Kinase', '', '', '', 'Transcription_Factor', '', '', 'IL-6 activation by TGF-beta1 was accompanied by nuclear translocation of NF-kappaB, which was blocked by the p38 inhibitors SB202190 and SB203580 or by IkappaBalphaDeltaN transfection, indicating the crucial role for the p38-NF-kappaB signaling in TGF-beta1 induction of IL-6.     ///    \"Transforming growth factor-beta1 activates interleukin-6 expression in prostate cancer cells through the synergistic collaboration of the Smad2, p38-NF-kappaB, JNK, and Ras signaling pathways.. \"    ///    \"Cotransfection assays demonstrated that TGF-beta1 stimulation of IL-6 results from the synergistic collaboration of the Smad2, p38-NF-kappaB, JNK-c-Jun-AP-1, or Ras-Raf-MEK1 cascades. \"'), ('9445', 'VIP_PACAP', '', 'VIP', 'PACAP', '10975815', '10', '', '', '', '', '', '', '', '', '', 'We showed previously that VIP/PACAP inhibit NF-kappaB nuclear translocation through the stabilization of IkappaB and reduce IFN regulatory factor-1 (IRF-1) binding to the regulatory elements found in the IL-12 p40 and inducible NO synthase promoters.     ///    \"In agreement with the described Janus kinase (Jak)1/Jak2/STAT1/IRF-1 activation pathway, VIP/PACAP inhibit Jak1/Jak2, STAT1 phosphorylation, and the binding of STAT1 to the GAS sequence motif in the IRF-1 promoter. \"    ///    In this paper we studied the molecular mechanisms involved in the VIP/PACAP regulation of IRF-1 transactivating activity.     ///    \"The effects of VIP/PACAP are mediated through the specific VIP/PACAP receptor-1 and the cAMP/protein kinase A (PKA) transduction pathway, but not through the induction of suppressor of cytokine signaling-1 or suppressor of cytokine signaling-3. \"'), ('9446', 'STAT3_JAK2', '', 'STAT3', 'JAK2', '26232730', '10', 'Huntington disease', '', 'Kinase', 'Oncogene', '', 'Receptor', 'Transcription_Factor', '', '', 'Finally, we will revise the anti-inflammatory pathway promoted via ?7 nAChR activation that is related to recruitment and activation of Jak2/STAT3 pathway, which on the one hand inhibits NF-?B nuclear translocation, and on the other hand, activates the master regulator of oxidative stress Nrf2/HO-1. '), ('9447', 'IGH_BCL2', '', 'IGH', 'BCL2', '15973455', '10', 'composite lymphoma;non Hodgkin Lymphoma', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'In the HL/FL and HL/MCL combinations, BCL2/IGH and CCND1/IGH translocations, respectively, were detected in both the HL and NHL.     ///    \"In conclusion, we present the first examples of molecularly verified IgH-associated translocations in HL, which also show that BCL2/IGH or CCND1/IGH translocations can represent early steps in the pathogenesis of composite HL/FL or HL/MCL. \"'), ('9448', 'BCL3_BCL10', '', 'BCL3', 'BCL10', '18628489', '10', 'MALT lymphoma;B cell lymphoma;lymphoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'the activated NF-kappaB up-regulated BCL10, and the activated AKT caused formation of BCL10/BCL3 complexes that translocated to the nucleus. '), ('9449', 'EIF4G_PABP1', '', 'EIF4G', 'PABP1', '19087191', '10', '', '', '', '', '', '', '', '', '', 'We showed here that in the heat-shocked cells, the PABP1-eIF4G complex dissociated, and both polypeptides translocated with the HSP27 to the nucleus.     ///    HSP27 remained associated with the eIF4G-PABP1 complex during recovery from heat shock. '), ('9450', 'PAK2_P85', '', 'PAK2', 'P85', '12226077', '10', '', '', 'Kinase', '', '', '', '', '', '', 'Our study defines a novel signaling pathway for bFGF-induced neurite outgrowth that involves activation of the PAK2-p85 betaPIX complex via the ERK cascade and subsequent translocation of this complex..    ///    Our study defines a novel signaling pathway for bFGF-induced neurite outgrowth that involves activation of the PAK2-p85 betaPIX complex via the ERK cascade and subsequent translocation of this complex.. '), ('9451', 'P65_P50', '', 'P65', 'P50', '7925300', '10', '', '', '', '', '', '', '', '', '', 'In HeLa cells as well as in B cells, TNF-alpha rapidly induced nuclear translocation primarily of p50-p65, but not of c-rel. '), ('9452', 'SREBP2_SCAP', '', 'SREBP2', 'SCAP', '24068000', '10', 'retinoblastoma\r\r', '', '', '', '', '', '', '', '', 'Interestingly, the expression levels of LDLr, SCAP, and SREBP-2 and the translocation of SCAP/SREBP-2 complex from the ER to the Golgi in treated VSMCs were decreased even in the presence of inflammatory stress.     ///    \"Results showed that inflammation increased lipid accumulation in aortas of ApoE KO mice and in VSMCs, which were correlated with increased expressions of LDLr, sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP), and SREBP-2 as well as with enhanced translocation of SCAP/SREBP-2 complex from the endoplasmic reticulum (ER) to the Golgi. \"'), ('9453', 'TMPRSS2_ERG', '', 'TMPRSS2', 'ERG', '24961351', '10', 'prostate cancer\r\r', 'FISH;PCR;RT-PCR ', '', '', '', '', '', 'KB', 'Seq', 'TMPRSS2-ERG has also been detected in prostate intraepithelial neoplasia (PIN) lesions and more rarely in benign prostatic hyperplasia (BPH) regions mainly in PCa-bearing glands.     ///    These findings indicate that TMPRSS2-ERG may or may not lead to PCa development..     ///    The possibility that the fusion TMPRSS2-ERG may be present in BPH samples in the absence of apparent PCa was addressed. '), ('9454', 'BCR_ABL1', '', 'BCR', 'ABL1', '25074248', '10', 'acute myeloid leukemia;myeloid leukemia;myelodysplastic syndrome;leukemia;hematopoietic malignancy\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'We describe a case of relapsed acute myeloid leukemia (AML) after HCT that developed a BCR-ABL1 translocation along with erythrophagocytosis by blasts as a secondary change at the time of relapse. '), ('9455', 'P65_P50', '', 'P65', 'P50', '22730546', '10', '', 'PCR', '', '', '', '', '', '', '', 'These effects were paralleled by a decrease in the nuclear translocation of NF-?B, as demonstrated by a decrease in the expression of MyD88, degradation of IRAK-1 and I?B? expression of the nuclear NF-?B p50/p65 subunits, p-p38 MAPK and p-MEK1, and NF-?B-dependent luciferase reporter gene activity in LPS-stimulated cells.     ///    \"Western blotting was used to assess the expression of the MyD88, the degradation of IRAK-1 and I?B?, the expression of the NF-?B p50/p65 subunits, the p-p38 MAPK and p-MEK1, as well as histone modifications. \"'), ('9456', 'P47_SRC', '', 'P47', 'SRC', '19892012', '10', 'lung inflammation', '', 'Kinase', '', '', '', '', '', '', 'Furthermore, CSE induced p47(phox) translocation and TLR4/MyD88/TRAF6 and c-Src/p47(phox) complex formation. '), ('9457', 'P65_NFKB1', '', 'P65', 'NFKB1', '19883646', '10', 'breast cancer\r\r', '', '', '', '', '', 'Transcription_Factor', '', '', 'Our data suggest that p53-dependent reactive oxygen species (ROS) induce p53-phosphorylation via p38MAPK in a feedback loop to inhibit IkappaBalpha-phosphorylation and NF-kappaB/p65 nuclear translocation, thereby down-regulating the metastatic proteins metalloproteinase (MMP)-2 and MMP-9. '), ('9458', 'PEG_IFN', '', 'PEG', 'IFN', '16042879', '10', 'hepatitis', 'PCR', '', '', '', '', '', '', '', 'The results suggested a trend that patients with genotype B HBV compared to genotype C had better SR to PEG-IFN therapy, although the difference was not significant.     ///    [Influences of the genotypes of HBV and HBeAg regarding their response to PEG-IFN in chronic hepatitis B patients]..     ///    \"Our results indicate that HBV genotype and HBeAg, especially the later, are main factors for predicting PEG-IFN therapy response in CHB patients.. \"'), ('9459', 'GPI_PLC', '', 'GPI', 'PLC', '16649989', '10', 'african trypanosomiasis', '', '', '', '', '', '', '', '', 'brucei to hypo-osmolarity or mild alkalinity, which also, strikingly, caused translocation of GPI-PLC from glycosomes (peroxisomes) to the ER.     ///    (c) translocation of GPI-PLC from glycosomes to the ER is important for in vivo cleavage of GPIs.     ///    We examined possible contributions of GPI-PLC to the response of T.     ///    We conclude that: (a) GPI-PLC contributes to loss of GPIs in T.     ///    Glycosome-to-ER movement of GPI-PLC reveals a novel pathway for intracellular protein traffic.     ///    A catalytically inactive Gln81Leu mutant of GPI-PLC failed to cleave GPIs despite being transported from glycosomes to the ER after hypo-osmotic or mild alkaline treatment of the parasites.     ///    (b) access of GPI-PLC to its substrate in vivo can be regulated post-translationally.     ///    (d) Cys347 is part of a peptide motif required for post-translational targeting of GPI-PLC to the ER. '), ('9460', 'TIM16_PAM18', '', 'TIM16', 'PAM18', '19564938', '10', '', '', '', '', '', '', '', '', '', 'The mitochondrial protein translocation motor: structural conservation between the human and yeast Tim14/Pam18-Tim16/Pam16 co-chaperones..     ///    We chose a structural approach in order to examine the evolutionary conservation between yeast Tim14/Pam18-Tim16/Pam16 proteins and their human homologues.     ///    Of particular interest for us is the human Tim14/Pam18-Tim16/Pam16 complex. '), ('9461', 'CCNB1_CDC2', '', 'CCNB1', 'CDC2', '10854050', '10', '', '', 'Kinase', '', '', '', '', '', '', 'This provides evidence that the activation of cdc2/cyclin B1 is initiated in the cytoplasm and that full activation of the translocated pool occurs in the nucleus..     ///    We provide evidence that a portion of the cdc2/cyclin B1 translocated into the nucleus in prophase is the inactive tyrosine-15-phosphorylated form.     ///    Centrosomal and cytoplasmic Cdc2/cyclin B1 activation precedes nuclear mitotic events..     ///    \"Here we demonstrate biochemically that cdc2/cyclin B1 accumulates at the centrosome in late G2 as the inactive, phosphotyrosine 15 form and that the centrosomal cdc2/cyclin B1 can be activated in vitro by recombinant cdc25B. \"    ///    At this time the centrosomal and cytoplasmic cdc2/cyclin B1 is already active.     ///    Cdc2/cyclin B1 accumulates at the centrosome in late G2 phase and has been implicated in the conversion of the centrosome from an interphase to a mitotic microtubule organizing center. '), ('9462', 'TIS21_PC3', '', 'TIS21', 'PC3', '11989967', '10', '', '', '', '', '', '', '', '', '', ' The antiproliferative B-cell translocation gene 2 (BTG2(TIS21/PC3)) is emerging as an important regulator of cell cycle dynamics.     ///    \"Our results therefore indicate an imperfect correlation between the terminally differentiated phenotype and BTG2(TIS21/PC3) expression, but no correlation between basal cellular proliferative or apoptotic indices and BTG2(TIS21/PC3) expression levels.. \"    ///    \"Highest levels of BTG2(TIS21/PC3) expression were seen in kidney proximal tubules, lung alveolar bronchial epithelium and in the basal cell layer of prostate acini. \"    ///    \"BTG2(TIS21/PC3) expression increases in response to the induction of DNA damage, cell differentiation, cell quiescence, cell contact, and as part of a positive feedback mechanism in response to growth stimulation. \"    ///    The objective of the present study was to provide further insight into the biological function of BTG2(TIS21/PC3) by determining the expression levels and cellular localization of BTG2(TIS21/PC3) in a spectrum of normal human tissues and to determine the proliferative indices (based on Ki-67 staining) and apoptotic indices (based on TUNEL assay) in those cell populations where BTG2(TIS21/PC3) was differentially expressed.     ///    BTG2(TIS21/PC3) was expressed at significantly different levels within the different epithelial populations of the kidney (proximal vs distal tubules) and prostate (acinar basal cells vs lumenal cells). '), ('9463', 'MAGI3_AKT1', '', 'MAGI3', 'AKT1', '22722202', '10', 'breast cancer', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'The MAGI3-AKT3 fusion leads to constitutive activation of AKT kinase, which is abolished by treatment with an ATP-competitive AKT small-molecule inhibitor.. '), ('9464', 'HRX_ALL1', '', 'HRX', 'ALL1', '10023690', '10', 'leukemia\r\r', '', '', '', '', '', '', '', '', ' The MLL (HRX/ALL-1 gene is frequently disrupted in infantile leukemias and therapy-related leukemias and fused to various translocation partner genes. '), ('9465', 'MLL_FOXO4', '', 'MLL', 'FOXO4', '21562049', '10', 'T cell leukemia', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', 'KB', '', 'Molecular analysis for translocations in MLL genes indicated that these AML patient-derived LICs all expressed the MLL-AFX1 fusion product. '), ('9466', 'MAPK14_JNK', '', 'MAPK14', 'JNK', '24871655', '10', '', '', 'Kinase', '', '', '', 'Transcription_Factor', '', '', 'These data demonstrate that magnolol inhibits TNF-?-induced JNK/p38 phosphorylation, HuR translocation, NF-?B activation, and thereby suppresses VCAM-1 expression resulting in reduced leukocyte adhesion.     ///    Magnolol reduced TNF-?-induced vascular cell adhesion molecule-1 expression in endothelial cells via JNK/p38 and NF-?B signaling pathways.. '), ('9467', 'EGFR_PRKDC', '', 'EGFR', 'PRKDC', '21266349', '10', '', '', 'Kinase', '', '', '', 'Transcription_Factor', '', '', 'EGFR-DNA-PKcs binding was induced by cisplatin or IR but not by EGFR nuclear translocation per se. '), ('9468', 'IkappaB-alpha_IKKbeta', '', 'IkappaB-alpha', 'IKKbeta', '17064662', '10', 'chronic obstructive pulmonary disease', '', '', '', '', '', '', '', '', 'The classical IKKbeta-IkappaBalpha and p38 MAPK pathways are involved in synergistic activation of NF-kappaB via two distinct mechanisms, p65 nuclear translocation-dependent and -independent mechanisms.     ///    \"pneumoniae is mediated by CK2, IKKbeta-IkappaBalpha, and p38 MAPK.. \"'), ('9469', 'GSTT1_GSTM1', '', 'GSTT1', 'GSTM1', '19009239', '10', 'lung cancer\r\r', 'PCR', '', '', '', '', '', '', '', 'The present study demonstrates that the presence of null genotype of GSTM1/GSTT1 taken together with CYP1A1 (Val/Val) genotype increases the susceptibility to LC eightfold in comparison to CYP1A1 (Ile/Ile) and GSTM1/ GSTT1 genotype.. '), ('9470', 'TAP2_TAP1', '', 'TAP2', 'TAP1', '8163941', '10', '', '', '', '', '', '', '', '', '', ' The major histocompatibility complex (MHC)-encoded heterodimeric TAP1/TAP2 transporter (TAP) translocates cytosolic peptides into the lumen of the endoplasmic reticulum (ER), where peptides of 8 to 11 amino acids long associate with MHC class I molecules. '), ('9471', 'EML4_ALK', '', 'EML4', 'ALK', '25841697', '10', 'non small cell lung cancer;breast cancer;lung cancer;melanoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'For instance, alterations in the epidermal growth factor receptor (EGFR) domain and echinoderm microtubule associated protein-like 4- anaplastic lymphoma kinase (EML4-ALK) translocation are routinely used to guide therapeutic decisions for advanced NSCLC.     ///    \"Several new treatments targeting EGFR family members, novel EML4-ALK inhibitors and MEK inhibitors are currently in clinical development. \"'), ('9472', 'P65_P50', '', 'P65', 'P50', '19445900', '10', '', '', '', '', '', '', '', '', '', 'Results obtained show that selected purified compounds had a cytotoxic effect on the human leukaemia cell line K562, inhibited both TNF-alpha-induced NF-kappaB-DNA binding as well as TNF-alpha-induced IkappaBalpha degradation and nuclear translocation of p50/p65. '), ('9473', 'P130_P107', '', 'P130', 'P107', '22473992', '10', 'sarcoma\r\r', '', '', '', '', '', '', '', '', 'Ligand-activated PPAR?/? repressed expression of these genes by direct binding with p130/p107, facilitating nuclear translocation and increasing promoter recruitment of p130/p107. '), ('9474', 'PI3K_HRAS', '', 'PI3K', 'HRAS', '25980493', '10', 'hepatocellular carcinoma\r\r', '', '', 'Oncogene', '', '', '', '', '', 'SOS1 activated the HRAS/PI3K/AKT pathway and resulted in nuclear translocation of p-AKT and Bcl-2.     ///    \"Finally, the activation of the HRAS/PI3K/AKT pathway by EGFR-induced SOS1 also inhibits cisplatin-induced apoptosis, suggesting a common apoptosis-evasion mechanism in hepatoma cells. \"'), ('9475', 'TLR4_LPS', '', 'TLR4', 'LPS', '25092897', '10', 'gastric cancer', '', '', '', '', '', '', '', '', 'AEG-1 was upregulated via LPS-TLR4 signaling and in turn promoted nuclear translocation of the NF-?B p65 subunit. '), ('9476', 'TNFA_IFNG', '', 'TNFA', 'IFNG', '9988719', '10', '', '', '', '', '', '', '', '', '', 'The PKR inhibitor 2-aminopurine (2-AP) inhibited TNF-alpha/IFN-gamma-induced NF-kappaB nuclear translocation in neuronal derived cells but not in endothelial cells.     ///    \"The induced degradation of IkappaBbeta, which is normally observed upon TNF-alpha/IFN-gamma cotreatment, was blocked completely by 2-AP in neuronal derived cells. \"    ///    \"Our results suggest that the signal generated by IFN-gamma during TNF-alpha/IFN-gamma cotreatment may require PKR to elicit enhanced NF-kappaB activity, and this signal may affect the stability of the IkappaBbeta protein.. \"    ///    \"therefore, we examined the possibility that PKR may play a role in the synergistic activation of NF-kappaB during TNF-alpha/IFN-gamma cotreatment. \"    ///    \"Also, 2-AP treatment or overexpression of a catalytically inactive PKR inhibited the TNF-alpha/IFN-gamma-induced synergistic activation of kappaB-dependent gene expression. \"'), ('9477', 'MAPK3_P42', '', 'MAPK3', 'P42', '11682603', '10', '', '', 'Kinase', '', '', '', '', '', '', ' We previously reported that nuclear translocation is essential for p42/p44 MAPKs (ERKs) mitogenic signaling.     ///    \"Hence, the nucleus is a critical site for mitogenic signal termination by: (1) nuclear sequestration of p42/p44 MAPKs away from MEK, their cytoplasmic activator. \"    ///    \"In addition, p42/p44 MAPKs permanently shuttle between the cytoplasm and the nucleus in quiescent as well as in serum stimulated cells. \"    ///    \"Here we show that, during long-term stimulation, p42/p44 MAPKs become inactive while they accumulate in the nucleus. \"    ///    \"The phosphatases responsible for p42/p44 MAPKs nuclear inactivation are neo-synthesized, show tyrosine or dual specificity, and interact with p42/p44 MAPKs via a specific docking site. \"    ///    \"This inactivation was monitored by phospho-specific immunostaining and dephosphorylation of a nuclear p42/p44 MAPKs substrate, HIF-1 alpha. \"'), ('9478', 'RAC2_MYH9', '', 'RAC2', 'MYH9', '25180062', '10', '', '', '', '', '', '', '', '', '', 'The level of induced Rac2-Myh9 interaction strongly correlated with the degree of HuR translocation. '), ('9479', 'NLS_GPCR', '', 'NLS', 'GPCR', '21371461', '10', '', '', '', '', '', '', '', '', '', 'Unlike wildtype GPCRs, in the presence of agonist/antagonist ligands the GPCR-NLS is retained at the cell surface, and following ligand removal, the GPCR-NLS translocated from the cell surface. '), ('9480', 'FLI_EWS', '', 'FLI', 'EWS', '17301523', '10', 'bone cancer', '', '', '', '', '', '', '', '', 'Advances in molecular biology have revealed common chromosomal translocations such as EWS-FLI 1 among Ewing sarcoma and related diseases such as primitive neuroectodermal tumor (PNET), so these are considered as Ewing sarcoma family tumor (ESFT). '), ('9481', 'OCT2_MATE1', '', 'OCT2', 'MATE1', '20883471', '10', '', '', '', '', '', '', '', '', '', 'Double-transfected MDCK cells expressing human OCT1/MATE1 or OCT2/MATE1: determinants of uptake and transcellular translocation of organic cations.. '), ('9482', 'FLI1_EWSR1', '', 'FLI1', 'EWSR1', '26765686', '10', 'ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', 'Seq', 'IGF-1R: The IGF-1R pathway is known to be deregulated by the EWSR1-FLI1 translocation which makes it a potential target for therapy. '), ('9483', 'WNT3A_EGF', '', 'WNT3A', 'EGF', '24562386', '10', '', '', '', '', '', '', '', '', '', 'Co-stimulation with Wnt3a and epidermal growth factor (Wnt3a/EGF) induced development of tubes consisting of intestinal epithelial cells by inducing expression of Arl4c, an Arf-like small GTP-binding protein, in three-dimensional culture, while stimulation with Wnt3a or EGF alone did not. '), ('9484', 'TPM3_ALK', '', 'TPM3', 'ALK', '22591683', '10', 'anaplastic large cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'ALK-positive anaplastic large cell lymphoma with TPM3-ALK translocation.. '), ('9485', 'H19_DMR', '', 'H19', 'DMR', '23863936', '10', '', '', '', '', '', '', '', '', '', 'Maternal-specific H19-DMR deletion results in activation of the Igf2-Igfr1 pathway, as shown by the translocation of phosphorylated FoxO3 (an inactive form) from nucleus to cytoplasm and the release of FoxO3-mediated cell cycle arrest, thus leading to increased activation, proliferation and eventual exhaustion of haematopoietic stem cells.     ///    \"We demonstrate that conditional deletion of the maternal but not the paternal H19-DMR reduces adult haematopoietic stem cell quiescence, a state required for long-term maintenance of haematopoietic stem cells, and compromises haematopoietic stem cell function. \"    ///    \"Similarly, genetic inactivation of Igf1r partly rescues the H19-DMR deletion phenotype. \"    ///    \"Mechanistically, maternal-specific H19-DMR deletion leads to Igf2 upregulation and increased translation of Igf1r, which is normally suppressed by H19-derived miR-675. \"    ///    \"A differentially methylated region upstream of H19 (H19-DMR), serving as the imprinting control region, determines the reciprocal expression of H19 from the maternal allele and Igf2 from the paternal allele. \"'), ('9486', 'P65_NFKB1', '', 'P65', 'NFKB1', '12592390', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'Employing immunoblot analysis, enzyme-linked immunosorbent assay, and gel shift assay, we demonstrate that EGCG treatment of the cells resulted in a significant dose- and time-dependent inhibition of UVB-mediated activation and nuclear translocation of a NF-kappaB/p65. '), ('9487', 'TEL_JAK2', '', 'TEL', 'JAK2', '10706877', '10', 'leukemia\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'Furthermore, the expression of a dominant negative form of Stat5A markedly interfered with the growth factor independence process mediated by TEL-Jak2 in Ba/F3 cells. '), ('9488', 'ETO_AML1', '', 'ETO', 'AML1', '20376583', '10', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', 'PCR', '', '', '', '', '', '', '', 'Comparative monitoring of MRD by RQ-PCR for the Wilms\' tumor gene 1(WT1) or specific translocation markers demonstrated that BAALC had similar kinetics as WT1, AML1/ETO and minor BCR/ABL, but not PML/RARA. '), ('9489', 'RAB5_GEF', '', 'RAB5', 'GEF', '18486601', '10', '', '', '', '', '', '', '', '', '', 'Tyr-phosphorylation signals translocate RIN3, the small GTPase Rab5-GEF, to early endocytic vesicles..     ///    \"Our present results suggest that a Ras GTPase(s) activated by tyrosine-phosphorylation signals interacts with the inhibitory RA domain, resulting in an active conformation of RIN3 as a Rab5-GEF and that RIN-unique RH domain constitutes a Rab5-binding region for the progress of GEF action.. \"    ///    \"Here, we found tyrosine-phosphorylation signals are involved in the Rab5-GEF activation. \"    ///    \"Rab5-GEFs share a conserved VPS9 domain for the GEF action, and RIN3 containing additional domains, such as Src-homology 2, RIN-family homology (RH), and Ras-association (RA), was identified as a new Rab5-GEF. \"'), ('9490', 'IGH_BCL2', '', 'IGH', 'BCL2', '21184290', '10', 'follicular lymphoma;B cell lymphoma;lymphoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'However, the pathological significance of BCL-2/IgH translocation, which is characteristic in FL, in newly diagnosed cases of this disease is not well understood.     ///    \"BL-like tumor cells harbored amplified c-MYC genes with BCL-2/IgH translocation, but FL-like cells solely had BCL-2/IgH translocation. \"'), ('9491', 'P65_NFKB1', '', 'P65', 'NFKB1', '12692090', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'Only at high concentrations, cPG enhanced TNF-alpha-induced cell death and inhibited TNF-alpha-induced IkappaB-alpha kinase (IKK) activation, IkappaB-alpha degradation, and NF-kappaB/p65 translocation, while promoting AP-1/c-jun phosphorylation. '), ('9492', 'NFKB1_IkappaB', '', 'NFKB1', 'IkappaB', '10037137', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'On the other hand, GFP-p105 (GFP-p50 with IkappaB gamma) localized only in the cytoplasm before stimulation and translocated to the nucleus with stimulant specificity similar to that of native NF-kappaB/IkappaB.     ///    It was suggested that this might be due to the existence of a limiting step where NF-kappaB is released from NF-kappaB/IkappaB by the proteasome.. '), ('9493', 'SGT1_HSP90', '', 'SGT1', 'HSP90', '21864708', '10', '', '', '', '', '', '', '', '', '', 'Altogether, our results suggest that S100A6-Ca(2+)-mediated Sgt1 dephosphorylation promotes its nuclear translocation, most likely due to disruption of the Sgt1-Hsp90 complex.. '), ('9494', 'TLS_CHOP', '', 'TLS', 'CHOP', '26897615', '10', 'liposarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Phase II study of amrubicin (SM-5887), a synthetic 9-aminoanthracycline, as first line treatment in patients with metastatic or unresectable soft tissue sarcoma: durable response in myxoid liposarcoma with TLS-CHOP translocation..     ///    One patient with metastatic myxoid liposarcoma with TLS-CHOP translocation had a durable response and received 40?cycles of amrubicin. '), ('9495', 'TRX_ADF', '', 'TRX', 'ADF', '9274857', '10', 'T cell leukemia', '', '', '', '', '', '', '', '', 'In the Fe-NTA model only, Northern and Western blot analyses of the kidney revealed induction of ADF/TRX (> 2.5-fold) after 16 hours and translocation of ADF/TRX from the cytoplasmic to nuclear fraction (> 3.5-fold) after 24 hours.     ///    \"Collectively, these data suggest that: (a) ADF/TRX is induced and translocated to nuclei by oxidative damage mediated by Fe-NTA in the renal proximal tubules. \"    ///    and (c) ADF/TRX is involved in the cellular defense mechanisms in vivo against oxidative damage..     ///    (b) induction of ADF/TRX is independent of tubular necrosis or sulfhydryl depletion.     ///    \"In ex vivo experiments using serial normal kidney frozen sections, it was found that renal proximal tubules with low expression of ADF/TRX were more vulnerable to oxidative stress mediated by Fe-NTA. \"    ///    Immunohistochemistry showed a patchy distribution of ADF/TRX in the normal renal proximal tubules.     ///    ADF/TRX is a conserved multifunctional reductant presumably associated with redox regulation of the cellular environment.     ///    \"In the present series of experiments, we studied the expression and intracellular localization of ADF/TRX in mouse kidney from two different renal tubular injury models: a free radical-associated model with ferric nitrilotriacetate (Fe-NTA) and a free radical-independent model with HgCl2. \"'), ('9496', 'PDGFRA_FIP1L1', '', 'PDGFRA', 'FIP1L1', '15166033', '10', 'myeloproliferative disease', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The former usually results from translocations involving chromosome 5q31-33, and the latter usually results from an interstitial deletion involving chromosome 4q12 (FIP1L1-PDGFRA). '), ('9497', 'P65_P50', '', 'P65', 'P50', '10903761', '10', '', '', '', '', '', '', '', '', '', 'CQ acted by reducing TNF-alpha mRNA accumulation without destabilizing its mRNA or interfering with NF-kappaB nuclear translocation or p50/p65 isoform composition of DNA-binding complexes.     ///    These data indicate that CQ inhibits TNF-alpha gene expression without altering translocation of NF-kappaB p50/p65 heterodimers. '), ('9498', 'MAG_GPI', '', 'MAG', 'GPI', '1971150', '10', 'myotonic dystrophy', '', '', '', '', '', '', '', '', 'Studies with additional hybrids containing deletions or translocations in chromosome 19 enabled us to localize RYR to 19q13.1 in a region distal to GPI/MAG and proximal to D19S18/DNF11. '), ('9499', 'CDK2_CCNE', '', 'CDK2', 'CCNE', '19561638', '10', '', '', 'Kinase', '', '', '', 'Transcription_Factor', '', '', 'Previous studies have shown that the human NPM\'s phosphorylation by cyclin E-cyclin-dependent kinase 2 (cdk2) on threonine (Thr) 199 regulates its translocation from the centrosome during cell cycle progression. '), ('9500', 'P65_NFKB1', '', 'P65', 'NFKB1', '20669099', '10', 'glioblastoma multiforme\r\r', '', '', '', '', '', 'Transcription_Factor', '', '', 'PKC alpha phosphorylates cytosolic NF-kappaB/p65 and PKC delta delays nuclear translocation of NF-kappaB/p65 in U1242 glioblastoma cells..     ///    PKC delta decelerated the nuclear translocation of activated NF-kappaB/p65 up to 4 hours after the stimulation.     ///    PKC delta delays the translocation of active NF-kappaB/p65 into the nucleus.     ///    PMA induced the phosphorylation of NF-kappaB/p65 by PKC alpha.     ///    PKC alpha is needed to phosphorylate NF-kappaB/p65.     ///    Gene silencing with siRNA against NF-kappaB/p65 inhibited [3H]-thymidine incorporation in U1242 GBM cells.     ///    NF-kappaB/p65 is pro-survival and proliferative factor in U1242 GBM cells.     ///    \"Gene silencing of PKC alpha , PKC delta and NFkappaB/ p65 with siRNA interference was utilized to evaluate their roles in NFkB activation and cell proliferation. \"    ///    PMA induced death was not observed in PKC delta silenced cells where activated NF-kappaB/p65 was located immediately in the nucleus.     ///    PMA-induced cell death occurred if the phospho-NF-kappaB/p65 was prohibited from entering the nucleus in PKC delta positive cells. '), ('9501', 'ZFP36L2_PRDM16', '', 'ZFP36L2', 'PRDM16', '21325596', '10', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', 'Transcription_Factor', '', '', 'Rare mutations of NRAS, FLT3-ITD, MLL-PTD, ERG amplification, and ZFP36L2-PRDM16 translocation, but no TP53, TET2, CBL, NPM1, and CEBP? mutations were found. '), ('9502', 'P62_SQSTM1', '', 'P62', 'SQSTM1', '24492006', '10', '', '', 'Kinase', '', '', '', '', '', '', 'Here we show that translocation of p62/Sqstm1 to invasive Salmonella precedes Ser351 phosphorylation.     ///    \"However, the detailed role of p62/Sqstm1 during xenophagy has remained unclear. \"    ///    \"simultaneously, p62/Sqstm1 is phosphorylated at Ser351, leading to inactivation of Keap1, which is responsible for degrading Nrf2. \"    ///    \"Furthermore, in addition to Ser351 phosphorylation, oligomerization of p62/Sqstm1 is also required for localization of Keap1 onto microbes, which is followed by Nrf2 activation. \"    ///    Our data reveal the sequential dynamics of p62/Sqstm1 in response to bacterial infection.     ///    \" Upon infection of a cell by Salmonella, p62/Sqstm1 assembles on the microbes. \"    ///    Dissection of the role of p62/Sqstm1 in activation of Nrf2 during xenophagy.. '), ('9503', 'ERK1_EGFR', '', 'ERK1', 'EGFR', '26133701', '10', '', '', 'Kinase', '', '', '', '', '', '', 'Activation of the P2Y6 receptor is also involved in radiation-induced activation of the epithelial growth factor receptor-extracellular signal regulated protein kinase (EGFR-ERK)1/2 pathway and subsequent nuclear translocation of EGFR, which plays a role in DNA repair. '), ('9504', 'P22_P21', '', 'P22', 'P21', '3871525', '10', '', '', '', '', '', '', '', '', '', 'A combination of regional mapping using a chromosome 1 translocation and comparative gene mapping suggests that the human NGF gene is in the p21-p22.1 region of chromosome 1. '), ('9505', 'HSL_CFP', '', 'HSL', 'CFP', '15456755', '10', '', '', '', '', '', '', '', '', '', 'In the presence of 20 microm forskolin, CFP-HSL translocated to the triacylglycerol droplet, coincident with BODIPY-FA labeled depots.     ///    \"In contrast, little if any fluorescence resonance energy transfer could be detected between CFP-HSL and YFP-liver FABP. \"    ///    Fluorescence resonance energy transfer analysis demonstrated that CFP-HSL associated with YFP-adipocyte FABP in both basal and forskolin-treated cells. '), ('9506', 'PRX1_NLS', '', 'PRX1', 'NLS', '17603937', '10', '', '', '', '', '', '', '', '', '', 'In contrast, increased NLS-Prx1 did not affect NF-kappaB nuclear translocation but increased activity of a NF-kappaB reporter.     ///    \"Both NLS-Prx1 and NES-Prx1 inhibited NF-kappaB p50 oxidation, suggesting that oxidation of the redox-sensitive cysteine in p50\'s DNA-binding domain is regulated via peroxide metabolism in both compartments. \"    ///    We targeted expression vectors to increase Prx1 in nuclei (NLS-Prx1) and cytoplasm (NES-Prx1) in HeLa cells.     ///    \"Interestingly, following treatment with H(2)O(2), nuclear thioredoxin-1 (Trx1) redox status was protected by NLS-Prx1, and cytoplasmic Trx1 was protected by NES-Prx1. \"'), ('9507', 'P47_Cortactin', '', 'P47', 'Cortactin', '24634221', '10', '', '', '', '', '', '', '', '', '', 'Furthermore, HGF stimulated p47(phox)/Cortactin/Rac1 translocation to lamellipodia and ROS generation. '), ('9508', 'RAC1_JNK', '', 'RAC1', 'JNK', '16927023', '10', '', '', '', '', '', '', '', '', '', 'This study is the first to demonstrate that H(2)O(2) induces a Rac1/JNK1/p38 signaling cascade, and that JNK and p38 activation is important for H(2)O(2)-induced apoptosis as well as AIF/Bax translocation of RPE cells.. '), ('9509', 'PAX3_FKHR', '', 'PAX3', 'FKHR', '19893043', '10', 'rhabdomyosarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', ' PAX3-FKHR is a fusion oncoprotein generated by the 2;13 chromosomal translocation in alveolar rhabdomyosarcoma (ARMS), a cancer associated with the skeletal muscle lineage.     ///    \"Although PAX3-FKHR alone failed to exert transforming activity, a combination of PAX3-FKHR and MYCN induced transforming activity in cell culture assays. \"    ///    \"Furthermore, myoblasts expressing PAX3-FKHR with or without MYCN formed tumors in SCID mice. \"    ///    Comparisons of tumor and parental cells revealed that only a subset of parental cells developed into tumors and that tumor cells expressed high PAX3-FKHR levels compared with transduced parental cells.     ///    High expression of the PAX3-FKHR oncoprotein is required to promote tumorigenesis of human myoblasts..     ///    \"To investigate the relationship between expression and phenotype in human myogenic cells, PAX3-FKHR was introduced into immortalized human myoblasts to produce a low overall PAX3-FKHR expression level. \"    ///    Previous studies determined that high-level PAX3-FKHR expression is a consistent feature in ARMS tumors.     ///    \"however, most subclones expressed low PAX3-FKHR and showed neither transforming nor tumorigenic activity. \"    ///    \"Finally, RNA interference experiments in myoblast-derived tumor and ARMS cells revealed that high PAX3-FKHR expression plays a crucial role in regulating proliferation, transformation, and differentiation. \"'), ('9510', 'SYT_SSX1', '', 'SYT', 'SSX1', '11487273', '10', 'synovial sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Twelve, 10 and 1 case carried the SYT-SSX1, SYT-SSX2 and SYT-SSX4 fusion transcript, respectively. '), ('9511', 'MYC_BCL2', '', 'MYC', 'BCL2', '25704881', '10', 'B cell lymphoma;B cell lymphoma;lymphoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'Furthermore, concurrent CXCR4+ and BCL2 translocation showed dismal outcomes resembling but independent of MYC/BCL2 double-hit DLBCL. '), ('9512', 'P65_P50', '', 'P65', 'P50', '24952412', '10', '', '', '', '', '', '', '', '', '', 'Treatment with lidocaine also significantly inhibited the phosphorylation of p38 MAPK and the nuclear translocation of NF-?B p50/p65, increased the protein levels of inhibitor kappa B-?. '), ('9513', 'PRB2_HDAC1', '', 'PRB2', 'HDAC1', '24658119', '10', 'retinoblastoma\r\r', '', '', '', '', '', 'Transcription_Factor', '', '', 'Additionally, RhoA inhibitors (statins) reversed the effect of 3MC in inhibiting DNA synthesis by decreasing the nuclear translocation of pRb2/HDAC1, leading to a recovery of the levels of cell-cycle regulatory proteins.     ///    \"Increased HDAC1/pRb2 recruitment to the E2F1 complex decreased E2F1-transactivational activity and H3/H4 deacetylation, resulting in the downregulation of cell-cycle regulatory proteins (Cdk2/4 and Cyclin D3/E). \"'), ('9514', 'WAF1_CIP1', '', 'WAF1', 'CIP1', '15004518', '10', 'retinoblastoma\r\r', '', '', '', '', '', '', '', '', 'In addition, p53 dephosphorylation coincided with caspase-3 activation, and translocation of p21(Cip1/Waf1) and p27(Kip1) into the cytoplasm, all of which were suppressed by caspase inhibition of TGF-beta1-induced apoptosis.     ///    p53 dephosphorylation and p21(Cip1/Waf1) translocation correlate with caspase-3 activation in TGF-beta1-induced apoptosis of HuH-7 cells..     ///    \"In conclusion, the results demonstrated that TGF-beta1-induced p53 dephosphorylation is associated with caspase-3 activation, and cytosolic translocation of p21(Cip1/Waf1) and p27(Kip1), resulting in decreased expression of Cdks and cyclins. \"    ///    \"This was associated with enhanced p53 dephosphorylation and p21(Cip1/Waf1) expression, which coincided with decreased Cdk2, Cdk4, and cyclin E expression, compared with synchronized G1 cells. \"'), ('9515', 'TRAF1_ALK', '', 'TRAF1', 'ALK', '25533804', '10', 'anaplastic large cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'A novel patient-derived tumorgraft model with TRAF1-ALK anaplastic large-cell lymphoma translocation..     ///    These data indicate that the activation of NFkB signaling contributes to the neoplastic phenotype of TRAF1-ALK ALCL.     ///    The treatment with proteasome inhibitors of TRAF1-ALK cells led to the downregulation of p50/p52 and lymphoma growth inhibition. '), ('9516', 'TFE3_LUC7L3', '', 'TFE3', 'LUC7L3', '24899691', '10', 'kidney cancer', '', '', '', '', '', '', '', '', 'Knockdown of INO80D decreased cell proliferation in a novel cell line bearing LUC7L3-TFE3 translocation. '), ('9517', 'SSX_SS18', '', 'SSX', 'SS18', '23716114', '10', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', ' Most synovial sarcomas contain a chromosomal translocation t(X;18), which results in the formation of an oncoprotein SS18-SSX critical to the viability of synovial sarcoma.     ///    Exploitation of SS18-SSX and its protein partners will allow us to develop potent tumor-specific therapeutic agents..     ///    \"In addition, we have identified a potential mediator of SS18-SSX function in exon 8. \"    ///    SS18-SSX represents a tumor-specific target in synovial sarcoma. '), ('9518', 'TR3_RXRA', '', 'TR3', 'RXRA', '14592536', '10', 'breast cancer;gastric cancer\r\r', '', '', '', '', 'Receptor', 'Transcription_Factor', '', '', 'In the present study, we found that formation of TR3/RXRalpha heterodimers in the nucleus and their subsequent translocation into the cytoplasm, in association with regulation of apoptosis-related proteins Bcl-2, Bcl-xl and Bax, was critical for apoptosis induction by ATRA in breast cancer cells MCF-7.     ///    \"In ATRA-induced MCF-7 cells, highly expressed TR3 favours the formation of TR3/RXRalpha and promotes the TR3/RXRalpha signalling pathway causing apoptosis. \"'), ('9519', 'MLL_ELL', '', 'MLL', 'ELL', '19932689', '10', 'leukemia\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'Acute myelogenous leukemia cells with the MLL-ELL translocation convert morphologically and functionally into adherent myofibroblasts.. '), ('9520', 'HBEGF_CTF', '', 'HBEGF', 'CTF', '20588025', '10', 'colon cancer\r\r', '', '', '', '', '', '', '', '', 'IL-8 induces cell proliferation and migration by an ADAM-dependent intranuclear translocation pathway of HB-EGF-CTF.     ///    \"Here, we focus on the mechanisms of IL-8-induced HB-EGF-CTF signaling, which is involved in cytoprotection and cellular repair.. \"'), ('9521', 'SYT_SSX2', '', 'SYT', 'SSX2', '21454665', '10', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Synovial sarcoma is an aggressive soft tissue tumor characterized by a chromosomal translocation between chromosome 18 and X, generating oncoproteins such as SYT-SSX1 and SYT-SSX2. '), ('9522', 'MAPK3_P42', '', 'MAPK3', 'P42', '9552382', '10', '', '', 'Kinase', '', '', '', '', '', '', 'Growth factors promote nuclear translocation and persistent activation of p42/p44 MAP kinases during the entire G0/G1 period.     ///    \"Here, we demonstrate that induction of cyclin D1, and therefore cdk4/6 activity associated with, is positively controlled by the p42/p44 MAP kinase cascade whereas the parallel cytokines/stress-activated p38MAP kinase cascade is antagonistic. \"    ///     Cell cycle re-entry requires the growth factor-stimulation of at least two distinct classes of protein kinases: (i) the p42/p44 MAP kinases activated by the Ras > Raf > MKK cascade and (ii) the G1 cyclin-dependent protein kinases (CDKs). '), ('9523', 'NOTCH1_HES1', '', 'NOTCH1', 'HES1', '18829436', '10', '', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', '', '', 'Our study indicated that SIRT1 is a player of repressing Notch1-Hes1 signaling pathway, and its transient translocation into the nucleus may have a role in the differentiation of NPCs.. '), ('9524', 'P65_NFKB1', '', 'P65', 'NFKB1', '15066217', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'alpha-Pinene pretreatment decreased the NF-kappa B/p65 nuclear translocation in LPS-stimulated THP-1 cells, and this effect was dose-dependent, but there was no reaction in LPS-unstimulated THP-1 cells.     ///    The expression of NF-kappa B/p65 in nuclei and that of I kappa B alpha in cytoplasm were measured by Western-blot analysis.     ///    The majority of FITC-labelled NF-kappa B/p65 was located in the nuclei being stimulated with LPS. '), ('9525', 'RUNX1_ETV6', '', 'RUNX1', 'ETV6', '20442364', '10', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia;down syndrome\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', '', 'We reviewed data from 2811 children with ALL enrolled in Children\'s Oncology Group P9900, which included prospective testing for the major cytogenetic lesions in childhood ALL: ETV6-RUNX1, TCF3-PBX1, BCR-ABL1, and MLL translocations and trisomies of chromosomes 4 and 10.     ///    \"However, when children with MLL translocations, BCR-ABL1, ETV6-RUNX1, and trisomies 4 and 10 were excluded, the EFS and OS were similar for children with and without DS (EFS 68.0 %+/- 9.3% vs 70.5% +/- 1.9%, P = .817. \"    ///    \"Children with DS-ALL had lower rates of the favorable cytogenetic lesions ETV6-RUNX1 (2.5% vs 24%, P < .001) and trisomies 4 and 10 (7.7% vs 24%, P < .001). \"'), ('9526', 'EML4_ALK', '', 'EML4', 'ALK', '26134230', '10', '', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Cystic Brain Metastases in NSCLC Harboring the EML4-ALK Translocation after Treatment with Crizotinib.. '), ('9527', 'EML4_ALK', '', 'EML4', 'ALK', '26750252', '10', 'anaplastic large cell lymphoma;non small cell lung cancer;lung cancer;neuroblastoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Expression of ALK in normal human tissues is only found in a subset of neural cells, however it is involved in the genesis of several cancers through genetic aberrations involving translocation of the kinase domain with multiple fusion partners (e.g., NPM-ALK in anaplastic large cell lymphoma ALCL or EML4-ALK in non-small cell lung cancer) or activating mutations in the full-length receptor resulting in ligand-independent constitutive activation (e.g., neuroblastoma). '), ('9528', 'SMAD4_SMAD2', '', 'SMAD4', 'SMAD2', '11278322', '10', '', '', '', '', 'Tumor_suppressor', '', 'Transcription_Factor', '', '', 'Lefty did not induce Smad2 or Smad5 phosphorylation, Smad2/Smad4 heterodimerization, or nuclear translocation of Smad2 or Smad4, but activated the MAPK pathway in a time- and dose-dependent fashion. '), ('9529', 'IRF4_CD10', '', 'IRF4', 'CD10', '21659362', '10', 'follicular lymphoma;B cell lymphoma;lymphoma\r\r', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', '', '', 'Both follicular lymphoma grade 3B and diffuse large B-cell lymphoma/follicular lymphoma grade 3B were enriched in samples with a CD10(-)IRF4/MUM1(+) immunophenotype (8/19, 42% and 7/16, 44%), with the vast majority of them lacking BCL2 translocations. '), ('9530', 'BCR_ABL1', '', 'BCR', 'ABL1', '21062244', '10', 'chronic myeloid leukemia;myeloid leukemia;leukemia\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', ' CML is characterized by the presence of the Philadelphia chromosome, which is the product of a reciprocal translocation between chromosomes 9 and 22 that results in the formation of BCR-ABL1.     ///    This underlines the importance of BCR-ABL1 at this stage of the disease.     ///    Apart from its diagnostic importance in CML patients BCR-ABL1 it is a potent oncogene.     ///    Clinical experience shows that long term remissions can be achieved at a high rate at least in chronic phase by specific inhibition of BCR-ABL1.     ///    \"How is BCR-ABL1 organized on the genetic level, is there a genetic precursor lesion as discussed for Philadelphia-negative myeloproliferative diseases, what is its role in pathogenesis and progression of CML and what is its role in the CML-stem cell? These questions will be discussed in this review.. \"'), ('9531', 'JUN_FOS', '', 'JUN', 'FOS', '25217162', '10', 'nocturnal enuresis', '', '', '', '', '', 'Transcription_Factor', '', '', 'It inhibits IL-10-driven nuclear translocation of c-Fos/c-Jun, critical for enhanced MDR-1 expression. '), ('9532', 'P18_AIMP3', '', 'P18', 'AIMP3', '22106287', '10', '', '', '', '', '', '', '', '', '', 'MRS also provides a cytosolic anchoring site for aminoacyl-tRNA synthetase-interacting multifunctional protein-3 (AIMP3)/p18, a potent tumor suppressor that is translocated to the nucleus for DNA repair upon DNA damage. '), ('9533', 'P65_NFKB1', '', 'P65', 'NFKB1', '11996111', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'Differential nuclear translocation of p65-NF-kappaB in LY sublines is due to the more efficient antioxidant defence in LY-S than in LY-R cells.. '), ('9534', 'P10_NTF2', '', 'P10', 'NTF2', '8955342', '10', '', '', '', '', '', '', '', '', '', ' p10/NTF2 is a cytosolic factor which is required for the translocation step in nuclear protein import in an in vitro assay with digitonin-permeabilized cells.     ///    \"To study the functional roles of p10/NTF2 on protein transport between the nucleus and cytoplasm in living cells, recombinant p10/NTF2 was micro-injected into cultured mammalian cells. \"    ///    Exogenously injected nuclear import factor p10/NTF2 inhibits signal-mediated nuclear import and export of proteins in living cells..     ///    Cytoplasmically injected p10/NTF2 strongly inhibited the nuclear import of co-injected NLS-containing substrates in a dose-dependent manner but had no effect on the diffusive import of small non-nuclear proteins.     ///    \"Moreover, when injected into the cell nucleus, p10/NTF2 inhibited the nuclear export of NES-containing substrates. \"    ///    The results suggest that the nuclear import factor p10/NTF2 may also be involved in the nuclear export of proteins and that the protein transport efficiency between the nucleus and cytoplasm may be regulated by the intracellular level of p10/NTF2.. '), ('9535', 'MEK_ERK', '', 'MEK', 'ERK', '10978848', '10', '', '', '', '', '', '', '', '', '', 'The Stats translocation did not depend on MEK-ERK inhibition by PD98059, inhibition of p38 by 1 microm SB203580, or Src kinase family inhibition by PP1. '), ('9536', 'MTOR_AMPK', '', 'MTOR', 'AMPK', '26329041', '10', 'non alcoholic fatty liver disease;nonalcoholic fatty liver disease', '', 'Kinase', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'Ghrelin upregulated autophagy via AMPK/mTOR restoration and inhibited translocation of NF-?B into the nucleus. '), ('9537', 'LZTS1_FEZ1', '', 'LZTS1', 'FEZ1', '17718912', '10', '', '', '', '', '', '', '', '', '', 'Activated Cdk1 complexes translocate into the nucleus during prophase where phosphorylate numerous substrates in order to enhance their activation as the cells progresses trough prophase, prometaphase, and metaphase.Recently we identified a new player: FEZ1/LZTS1 that contributes to the fine-tuning of the molecular events that determine progression through mitosis, and here will review its role in cancer development and in M phase regulation..     ///    Fez1/Lzts1 a new mitotic regulator implicated in cancer development.. '), ('9538', 'PTB2_FE65', '', 'PTB2', 'FE65', '18453713', '10', '', '', '', '', '', '', '', '', '', 'The interaction of the AICD with the C-terminal phosphotyrosine-binding domain of Fe65 (Fe65-PTB2) regulates APP translocation, signalling and processing.     ///    \"Human AICD and Fe65-PTB2 have been cloned, overproduced and purified in large amounts in Escherichia coli. \"    ///    A complex of Fe65-PTB2 with the C-terminal 32 amino acids of the AICD gave well diffracting hexagonal crystals and data have been collected to 2.1 A resolution. '), ('9539', 'BCR_ABL1', '', 'BCR', 'ABL1', '16683885', '10', 'leukemia;hematologic malignancy\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The identification of the Philadelphia chromosome and the subsequent discovery that it represents a translocation between the long arms of chromosomes 9 and 22 producing an aberrant tyrosine kinase, known as BCR-ABL1, has catalyzed our understanding and treatment of this hematologic malignancy.     ///    These inhibitors appear effective in inhibiting most of the mutant BCR-ABL1 molecules that are resistant to IM.     ///    \"The dominant mechanism appears to be mutations in the kinase domain of BCR-ABL1, which result in altered affinity of IM for the BCR-ABL1 protein. \"    ///    \"An extensive search for molecules to block the aberrant BCR-ABL1 protein resulted in the development of IM as an orally bioavailable agent with remarkable efficacy in producing hematologic, cytogenetic, and molecular remissions. \"'), ('9540', 'BCR_ABL1', '', 'BCR', 'ABL1', '18612408', '10', 'leukemia;hematologic malignancy\r\r', 'FISH;PCR;RT-PCR ', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Moreover, by immunoblotting and flow cytometry, we show that phosphorylation of BCR-ABL1 is increased in AQP5-overexpressing CML cells and decreased in AQP5 siRNA-treated CML cells. '), ('9541', 'ETO_AML1', '', 'ETO', 'AML1', '22687981', '10', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', ' Translocation (8;21)/AML1-ETO is considered a favorable cytogenetic abnormality in acute myeloid leukemia (AML).     ///    The therapeutic benefit of tyrosine-kinase inhibitor (TKI) was estimated by quantitative analysis of AML1-ETO and the patient\'s clinical impression.     ///    [Treatment with a tyrosine-kinase inhibitor of for c-KIT mutation and AML1-ETO double positive refractory acute myeloid leukemia]..     ///    \"However, patients with refractory AML associated KIT mutations in AML1-ETO should not be considered for TKI monotherapy.. \"    ///    \"However, the outcomes associated with KIT mutations in AML1-ETO have not been elucidated. \"'), ('9542', 'P65_ERK', '', 'P65', 'ERK', '17189385', '10', 'breast cancer\r\r', '', '', '', '', '', '', '', '', 'In contrast, both interaction and nuclear translocation of p65/ERK were reduced. '), ('9543', 'P65_P50', '', 'P65', 'P50', '24022118', '10', '', '', '', '', '', '', '', '', '', 'Annexin A6 interacted with p65, and loss of Anxa6 caused decreased nuclear translocation and retention of the active p50/p65 NF-?B complex. '), ('9544', 'SIRT1_AMPK', '', 'SIRT1', 'AMPK', '23657807', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'Through activation of SIRT1/AMPK pathway, monacolin K increased phosphorylation of acetyl CoA carboxylase and caused nuclear translocation of forkhead box O1.     ///    Monacolin K affects lipid metabolism through SIRT1/AMPK pathway in HepG2 cells..     ///    \"In summary, monacolin K reduces the lipid content through SIRT1/AMPK pathway in HepG2 cells, which promotes catabolism and inhibits anabolism of lipid. \"'), ('9545', 'PWCR1_HBII-85', '', 'PWCR1', 'HBII-85', '18320030', '10', 'hypogonadism', '', '', '', '', '', '', '', '', 'Our previous translocation studies predicted a major role for the C/D box small nucleolar RNA cluster SNORD116 (PWCR1/HBII-85) in PWS. '), ('9546', 'PTD_MLL', '', 'PTD', 'MLL', '24611505', '10', '', '', '', '', '', '', '', '', '', 'The kinetics of MLL-PTD relapses was both significantly slower than those of MLL translocation positive ones (median doubling time: MLL-PTD: 24?d, MLL-translocations: 12?d, P?=?0??015, Wilcoxon rank sum test), and displayed greater variation depending on additional mutations.     ///    \"As rapid relapses occurred in all MLL subgroups, frequent sampling are necessary to obtain acceptable relapse detection rates and times from molecular relapse to haematological relapse (blood sampling every second month: MLL-PTD: 75%/50?d. \"'), ('9547', 'P53_WOX1', '', 'P53', 'WOX1', '15580310', '10', 'breast cancer\r\r', '', '', '', '', '', '', '', '', 'We determined here that E(2) increased the formation of p53/WOX1 complex and their nuclear translocation in COS7 cells. '), ('9548', 'IGH_BCL2', '', 'IGH', 'BCL2', '21491965', '10', 'B cell lymphoma;lymphoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'In this article, we report a case of an adolescent patient who presented with high-grade breast lymphoma with concurrent BCL2-IGH and MYC-IGL translocations, and we review the clinical, pathological, and genetic features.     ///    Both primary breast lymphoma and lymphoma with concurrent BCL2-IGH and MYC translocations are rare and are primarily seen in adult patients. '), ('9549', 'CCNB1_CDK1', '', 'CCNB1', 'CDK1', '11063929', '10', '', '', 'Kinase', '', '', '', '', '', '', ' Nuclear events of mitosis are initiated when the protein kinase cyclin-B1-Cdk1 is translocated into the nucleus during prophase.     ///    Control of mitosis by changes in the subcellular location of cyclin-B1-Cdk1 and Cdc25C..     ///    Recent work has unveiled many of the mechanisms that govern the localization of cyclin-B1-Cdk1 and its regulator Cdc25C. '), ('9550', 'CCNB1_CDC2', '', 'CCNB1', 'CDC2', '9868363', '10', '', '', 'Kinase', '', '', '', '', '', '', 'These mechanisms are likely to make the mitotic activation of CDC2 (which is accompanied by the nuclear translocation of both CDC2-cyclin-B1 and its activator, CDC25C) and the growth-factor-induced activation of MAP kinase (which, upon sustained activation, concentrates in the nucleus and might thereby partially saturate the relevant MAP-kinase phosphatases) more switch-like.. '), ('9551', 'P62_SQSTM1', '', 'P62', 'SQSTM1', '23901824', '10', '', '', 'Kinase', '', '', '', '', '', '', 'Simvastatin-treated HL-1 cells exhibited mitochondrial translocation of Parkin and p62/SQSTM1, fission, and mitophagy. '), ('9552', 'WWTR1_CAMTA1', '', 'WWTR1', 'CAMTA1', '24798168', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'Epithelioid haemangioendothelioma of the uterine cervix with CAMTA1/WWTR1 translocation.. '), ('9553', 'MEK_ERK', '', 'MEK', 'ERK', '18941249', '10', 'renal cell carcinoma', '', '', '', '', '', '', '', '', 'Furthermore, we provide evidence that the intracellular signaling cascade responsible for VEGF-D up-regulation by CD74 is both PI3K/AKT- and MEK/ERK-dependent, both of which are associated with NF-kappaB nuclear translocation and DNA-binding activity. '), ('9554', 'ROCK_PTEN', '', 'ROCK', 'PTEN', '25520072', '10', 'gastric cancer\r\r', '', '', '', 'Tumor_suppressor', '', '', '', '', 'Ursolic acid promotes apoptosis of SGC-7901 gastric cancer cells through ROCK/PTEN mediated mitochondrial translocation of cofilin-1..     ///    Further mechanistic studies revealed that the ROCK1/PTEN signaling pathway plays a critical role in UA-mediated mitochondrial translocation of cofilin-1 and apoptosis. '), ('9555', 'CBF_AML1', '', 'CBF', 'AML1', '9291089', '10', '', '', '', '', '', '', '', '', '', 'During myelopoiesis, which includes the development of granulocytic and monocytic lineages, transcription factors from several families are active, including AML1/CBF beta, C/EBP, Ets, c-Myb, HOX, and MZF-1. '), ('9556', 'MEK_ERK', '', 'MEK', 'ERK', '15632293', '10', '', '', '', '', '', '', '', '', '', 'In response to stimulation, dissociation of the MEK-ERK complex is induced and activated ERK translocates to the nucleus. '), ('9557', 'BCR_ABL1', '', 'BCR', 'ABL1', '20231813', '10', 'megakaryocytic leukemia', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'We describe the first pediatric patient presenting with megakaryocytic leukemia and having BCR-ABL1 translocation as the single chromosomal abnormality. '), ('9558', 'WAF1_CIP1', '', 'WAF1', 'CIP1', '17429006', '10', '', '', '', '', '', '', '', '', '', 'In this study, we examined the posttranscriptional regulation of p21(CIP1/WAF1) after Fe depletion and demonstrated that its down-regulation was due to 2 mechanisms: (1) inhibited translocation of p21(CIP1/WAF1) mRNA from the nucleus to cytosolic translational machinery.     ///    \"We observed that Fe depletion increased the mRNA of the universal cyclin-dependent kinase inhibitor, p21(CIP1/WAF1), while its protein level was not elevated. \"    ///    \"In Fe-replete cells, p21(CIP1/WAF1) was degraded in an ubiquitin-dependent manner, while after Fe depletion, ubiquitin-independent proteasomal degradation occurred. \"    ///    Iron chelation significantly (P < .01) decreased p21(CIP1/WAF1) protein half-life from 61 (+/- 4 minutes.     ///    \"Proteasomal inhibitors rescued the chelator-mediated decrease in p21(CIP1/WAF1) protein, while lysosomotropic agents were not effective. \"    ///    \"This observation is unique to the G(1)/S arrest seen after Fe deprivation, as increased p21(CIP1/WAF1) mRNA and protein are usually found when arrest is induced by other stimuli. \"'), ('9559', 'P65_NFKB1', '', 'P65', 'NFKB1', '10461759', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'We conclude that differential nuclear translocation of p65-NF-kappaB in LY sublines is not related to the lethal effect of the activating, damaging agent.     ///    \"Hydrogen peroxide, phorbol ester and x-rays caused a marked translocation of p65-NF-kappaB in LY-R cells and a weak translocation in LY-S cells. \"    ///    \"By manipulating the antioxidant defense status, we obtained an alteration in the p65-NF-kappaB translocation induction in LY-R cells. \"'), ('9560', 'DUX4_CIC', '', 'DUX4', 'CIC', '23834194', '10', '', '', '', '', '', '', '', '', '', 'CD99-positive undifferentiated round cell sarcoma diagnosed on fine needle aspiration cytology, later found to harbour a CIC-DUX4 translocation: a recently described entity.. '), ('9561', 'PPARG_PAX8', '', 'PPARG', 'PAX8', '26259532', '10', 'papillary carcinoma;thyloid cancer\r\r', '', '', '', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'Some somatic oncogene mutations (BRAF, NRAS, HRAS, KRAS) as well as gene translocations (RET/PTC, PAX8/PPAR-gamma) have been associated with the development of thyroid cancer. ');
INSERT INTO `ChimerPub_dump` VALUES ('9562', 'EWS_ERG', '', 'EWS', 'ERG', '21623206', '10', 'small cell carcinoma\r\r', '', '', '', '', '', '', '', '', 'This was excluded by molecular studies that showed no evidence of EWS/FLI-1 or EWS/ERG translocation.. '), ('9563', 'CD18_CD11B', '', 'CD18', 'CD11B', '1358917', '10', '', '', '', '', '', '', '', '', '', ' Chemotactic stimulation of neutrophils results in translocation of CD11b/CD18 (Mac-1) from intracellular storage pools to the cell surface.     ///    Recruitment of CD11b/CD18 to the neutrophil surface and adherence-dependent cell locomotion.. '), ('9564', 'P65_NFKB1', '', 'P65', 'NFKB1', '16227413', '10', 'prostate cancer\r\r', '', '', '', '', '', 'Transcription_Factor', '', '', 'The results showed that YC-1 abolished constitutive nuclear translocation and activation of NF-kappaB/p65. '), ('9565', 'NRF2_HO1', '', 'NRF2', 'HO1', '26232730', '10', 'Huntington disease', '', '', '', '', '', '', '', '', 'Finally, we will revise the anti-inflammatory pathway promoted via ?7 nAChR activation that is related to recruitment and activation of Jak2/STAT3 pathway, which on the one hand inhibits NF-?B nuclear translocation, and on the other hand, activates the master regulator of oxidative stress Nrf2/HO-1. '), ('9566', 'P53_ROS', '', 'P53', 'ROS', '24482097', '10', 'breast cancer\r\r', '', '', '', '', '', '', '', '', 'the first phase of ROS was instrumental in ensuring activation of p53 via p38MAPK and its nuclear translocation for transactivation of Bax, which induced a second phase of mitochondrial ROS to construct the ROS-p53 feedback loop.     ///    Contribution of the ROS-p53 feedback loop in thuja-induced apoptosis of mammary epithelial carcinoma cells..     ///    \"Notably, under these conditions, thuja-induced breast cancer cell apoptosis was reduced, thereby validating the existence of an ROS-p53 feedback loop. \"'), ('9567', 'HEK_C5L2', '', 'HEK', 'C5L2', '19615750', '10', '', '', '', '', '', '', '', '', '', 'beta-Arrestin-2-GFP transiently transfected C5L2-HEK cells demonstrated rASP and rC5a-dependent beta-arrestin-2-GFP translocation, which showed time-dependent intracellular colocalization with C5L2.     ///    stably transfected C5L2-HEK cells were sorted using fluorescent-ASP (Fluos-ASP) binding. '), ('9568', 'IG_BCL2', '', 'IG', 'BCL2', '14737118', '10', 'follicular lymphoma;lymphoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'The actual sequence in the binding pocket matches the Bcl-2-Ig fusion sequence X06487, originally identified in a t(14:18) translocation of the Bcl-2 gene, associated with follicular lymphoma. '), ('9569', 'MALT1_API2', 't(11;18)(q21;q21) / ', 'MALT1', 'API2', '20081812', '10', 'MALT lymphoma;non Hodgkin lymphoma;lymphoma\r\r', '', '', '', '', '', '', '', '', 'It results in the creation of a fusion protein API2-MALT1 that activates the transcription factor NF-kappaB through enhanced IKK gamma polyubiquitination. '), ('9570', 'P65_NFKB1', '', 'P65', 'NFKB1', '18571841', '10', 'prostate cancer;lung cancer\r\r', '', '', '', '', '', 'Transcription_Factor', '', '', 'Degradation of IkappaBalpha was observed in all three cell lines, allowing NF-kappaB/p65 translocation to the nucleus. '), ('9571', 'RET_PTC1', '', 'RET', 'PTC1', '26695504', '10', 'thyroid nodule;thyloid cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'Mutations for KRAS, HRAS and NRAS and for BRAF and translocations of PAX8/PPAR?, RET/PTC1 and RET/PTC3 were investigated. '), ('9572', 'ZYX_RFP', '', 'ZYX', 'RFP', '12154072', '10', '', '', '', '', '', '', '', '', '', 'Using dual imaging of RFP-zyxin and GFP-alpha-actinin, we observed a temporal and spatial relationship between alpha-actinin localization to focal contacts and the subsequent disassembly or translocation of RFP-zyxin containing focal complexes in areas of cell retraction.     ///    \"Evidence is now provided that inhibiting calpain through over-expression of the endogenous inhibitor of calpain, calpastatin, and pharmacological inhibitors results in an inhibition of adhesive complex disassembly with stabilization of GFP-vinculin and GFP/RFP-zyxin at the cell periphery. \"'), ('9573', 'SLC45A3_ELK4', '', 'SLC45A3', 'ELK4', '22719019', '10', 'prostate cancer\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'The SLC45A3-ELK4 fusion, but not wild-type, ELK4 plays important roles in regulating cell growth in both androgen-dependent and -independent prostate cancer cells.     ///    \"With the absence of corresponding DNA rearrangement, chimeric fusion SLC45A3-ELK4 transcript in prostate cancer cells is generated by cis-splicing of adjacent genes/gene read-through instead of trans-splicing. \"    ///    \"Here, we show that a chimeric SLC45A3-ELK4 RNA is generated in the absence of chromosomal rearrangement. \"    ///    \"SLC45A3-ELK4 controls prostate cancer cell proliferation, and the chimera level correlates with prostate cancer disease progression.. \"'), ('9574', 'BCL2_IGH', '', 'BCL2', 'IGH', '12649152', '10', 'B cell lymphoma;lymphoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'and (2) is there a characteristic biologic background? In 10 of 13 DLBCL patients with relapse after 4 to 17 years, a clonal relationship was established based on identical IgH-sequences and/or identical bcl2-IgH translocation. '), ('9575', 'MYC_IG', '', 'MYC', 'IG', '18460403', '10', 'B cell lymphoma;lymphoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', ' The characteristics of de novo diffuse large B-cell lymphoma (DLBCL) with translocation of c-myc and immunoglobulin (Ig) genes (c-myc/Ig DLBCL), were investigated in 13 cases of c-myc/Ig DLBCL.     ///    \"These results suggest a heterogeneous immunophenotype and genotype for c-myc/Ig DLBCL, with CD10(-)/BCL6(+)/MUM1(-) cases the most frequent.. \"'), ('9576', 'MAPK3_P42', '', 'MAPK3', 'P42', '10668472', '10', '', '', 'Kinase', '', '', '', '', '', '', 'Preliminary data on hyperoxic signaling indicate that NF-kappa B translocation (and presumptive activation) is not a result of the p42/p44 MAPK pathway, but a likely downstream consequence of activation of the JNK pathway. '), ('9577', 'PRB_CDK6', '', 'PRB', 'CDK6', '27138926', '10', 'frontotemporal dementia;frontotemporal lobar degeneration;TDP-43 proteinopathies', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'We report here that both CK-1? inhibitors (IGS-2.7 and IGS-3.27) normalized the proliferative activity of PGRN-deficient lymphoblasts by preventing the phosphorylation of TDP-43 fragments, its nucleo-cytosol translocation and the overactivation of the CDK6/pRb cascade.     ///    \"Previous works from our laboratory described the presence of CDK6/pRb-dependent cell cycle alterations, and cytosolic accumulation of TDP-43 protein in lymphoblast from FTLD-TDP patients carriers of a loss-of function mutation in GRN gene (c.709-1G??>??). \"'), ('9578', 'P65_P50', '', 'P65', 'P50', '15547942', '10', '', '', '', '', '', '', '', '', '', 'As(2)O(3) suppressed DNA-binding activity of NF-kappaB composed of p65/p50 heterodimer through preventing the degradation of IkappaB-alpha and the nuclear translocation of p65 subsequently as well as interrupting the binding of NF-kappaB with their consensus sequences. '), ('9579', 'RUNX1_ETV6', '', 'RUNX1', 'ETV6', '21145270', '10', '', '', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', '', 'Febrile infections in young children do not frequently induce translocation ETV6-RUNX1.. '), ('9580', 'SAPK_JNK', '', 'SAPK', 'JNK', '11208906', '10', 'alzheimer disease\r\r', '', '', '', '', '', '', '', '', 'However, in control patients with some pathology, as well as in mild AD cases, there was nuclear phospho-JNK/SAPK and translocation of phospho-JNK/SAPK from nuclei to cytoplasm, respectively, indicating that the activation and re-distribution of JNK/SAPK correlates with the progress of the disease.     ///    \"Together, these findings suggest that JNK/SAPK dysregulation, probably resulting from oxidative stress, plays an important role in the increased phosphorylation of cytoskeletal proteins found in AD.. \"    ///    \"In this regard, in hippocampal and cortical regions of individuals with severe AD, the activated phospho-JNK/SAPK was localized exclusively in association with neurofibrillar alterations including neurofibrillary tangles, senile plaque neurites, neuropil threads and granulovacuolar degeneration structures (GVD), completely overlapping with tau-positive neurofibrillary pathology, but was virtually absent in these brain regions in younger and age-matched controls without pathology. \"    ///    \"By immunoblot analysis, phospho-JNK/SAPK is significantly increased in AD over control cases. \"'), ('9581', 'MYC_IGH', '', 'MYC', 'IGH', '16400328', '10', '', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'Role of genomic instability and p53 in AID-induced c-myc-Igh translocations..     ///    \"Finally, we demonstrate that accumulation of AID-dependent, IgH-associated chromosomal lesions is not sufficient to enhance c-myc-Igh translocations. \"'), ('9582', 'NTRK3_ETV6', '', 'NTRK3', 'ETV6', '25439992', '10', 'acinic cell carcinoma;adenocarcinoma\r\r', '', 'Kinase', '', '', '', '', 'KB', 'Seq', 'Diagnostic was confirmed by highlighting the ETV6-NTRK3 gene translocation. '), ('9583', 'RFP_GRX3', '', 'RFP', 'GRX3', '25975981', '10', '', '', '', '', '', '', '', '', '', 'Both fluorescence imaging of Grx3-RFP fusion and Western blot analysis of cellular fractionation indicate that Grx3 is predominantly localized in the cytoplasm under normal growth conditions, whereas under oxidizing conditions, Grx3 is translocated into and accumulated in the nucleus. '), ('9584', 'RAB8A_AS160', '', 'RAB8A', 'AS160', '23274898', '10', 'insulin resistance', '', '', '', '', '', '', '', '', 'ATP caused translocation of GLUT4myc-eGFP to the cell surface, mechanistically mediated by increased exocytosis involving AS160/Rab8A reduced by dominant-negative Akt or PI3K? kinase-dead mutants, and potentiated by myristoylated PI3K?. '), ('9585', 'LPS_IFNG', '', 'LPS', 'IFNG', '18818879', '10', '', '', '', '', '', '', '', '', '', 'Moreover, overexpression of kinase-inactive CK2 decreased iNOS expression and a significant amount of CK2alpha1 translocated into the nucleus in LPS/IFN-gamma-treated cells.     ///    We examined the regulatory role of Ikaros in LPS/IFN-gamma-induced inducible nitric oxide synthase (iNOS) expression by macrophages.     ///    \"Ikaros DNA binding activity on the iNOS promoter was decreased, and a mutation of the Ikaros-binding site on the iNOS promoter resulted in an increase in LPS/IFN-gamma-induced iNOS expression. \"    ///    Treatment with a casein kinase 2 (CK2) inhibitor reversed LPS/IFN-gamma-induced decrease in Ikaros DNA binding activity.     ///    \"Overall, these data indicate that LPS/IFN-gamma decreases the Ikaros DNA binding activity via the CK2 pathway, resulting in an increase of iNOS expression.. \"    ///    LPS/IFN-gamma increased the histone (H3) acetylation on the Ikaros DNA binding site. '), ('9586', 'Q10_P10', '', 'Q10', 'P10', '26715864', '10', 'polycystic ovary syndrome', '', '', '', '', '', '', '', '', 'Mrs HM had balanced translocation, 46XX t (7:11) (p10:q10). '), ('9587', 'DLX6_DLX5', '', 'DLX6', 'DLX5', '25196357', '10', '', '', '', '', '', '', '', '', '', 'In most cases, SHFM1 results from heterozygous deletions encompassing DLX5/DLX6 genes or from inversions and translocations separating the genes from their limb specific enhancers. '), ('9588', 'ATPase_ATP7A', '', 'ATPase', 'ATP7A', '23963605', '10', 'liver disease', '', '', '', '', '', '', '', '', 'It has been proposed that copper transporter 1 (CTR1) and the divalent metal transporter 1 (DMT1) translocate copper across the human intestinal epithelium, while Cu-ATPases: ATP7A and ATP7B serve as copper efflux pumps. '), ('9589', 'P300_CBP', '', 'P300', 'CBP', '26785692', '10', 'neuroblastoma\r\r', '', '', '', '', '', '', '', '', 'We found that nuclear translocation and acetylation of GAPDH increased in the presence of 5 mM Hcy and that higher levels of acetyltransferase p300/CBP were detected in Neuro2a cells. '), ('9590', 'TMPRSS2_ERG', '', 'TMPRSS2', 'ERG', '19002169', '10', 'prostate cancer\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'Many components of the epigenetic machinery, including histone deacetylase (whose expression level is linked to the TMPRSS2:ERG translocation) and the histone methylase EZH2, are potential therapeutic targets. '), ('9591', 'MET_ALK', '', 'MET', 'ALK', '22664824', '10', 'anaplastic large cell lymphoma;rhabdomyosarcoma;renal cell carcinoma;breast cancer;adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'A recent phase I dose-escalation trial of the selective MET/ALK inhibitor crizotinib showed a long-term partial response in a patient with IMT carrying an ALK translocation but not in a patient with ALK-negative disease. '), ('9592', 'P50_NFKB1', '', 'P50', 'NFKB1', '18922932', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'We also observed that delphinidin treatment of cells resulted in a dose-dependent decrease in (a) phosphorylation of IkappaB kinase gamma (NEMO), (b) phosphorylation of nuclear factor-kappaB (NF-kappaB) inhibitory protein IkappaBalpha, (c) phosphorylation of NF-kappaB/p65 at Ser(536) and NF-kappaB/p50 at Ser(529), (d) NF-kappaB/p65 nuclear translocation, and (e) NF-kappaB DNA binding activity. '), ('9593', 'CTNNB1_APC', '', 'CTNNB1', 'APC', '11823972', '10', 'fibromatoses', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', '', '', 'These findings indicate that alterations of the APC/beta-catenin pathway with resultant nuclear translocation of beta-catenin are important in the pathogenesis of both sporadic and FAP-associated breast fibromatosis.     ///    \"Somatic alterations of the APC/beta-catenin pathway were detected in 79% of breast fibromatoses, including activating beta-catenin gene mutations in 15 cases and somatic APC alterations (mutation or 5q allelic loss or both) in 11. \"    ///    \"However, their occasional occurrence in patients with familial adenomatous polyposis (FAP) and their morphologic identification with other deep fibromatoses (desmoid tumors) suggest that alterations of the APC/beta-catenin pathway might be involved in the pathogenesis of sporadic and FAP-associated breast fibromatoses. \"    ///    Fibromatosis of the breast and mutations involving the APC/beta-catenin pathway.. '), ('9594', 'EML4_ALK', '', 'EML4', 'ALK', '20418096', '10', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'More recently ALK inhibitors have entered clinical development and remarkably clinical efficacy has been observed in NSCLC patients harbouring EML4-ALK translocations.     ///    The biology and treatment of EML4-ALK non-small cell lung cancer..     ///    EML4-ALK is oncogenic both in vitro and in vivo and ALK kinase inhibitors are quite effective in pre-clinical model systems.     ///    EML4-ALK is most often detected in never smokers with lung cancer and has unique pathologic features.     ///    \"This review will focus on the biology, clinical characteristics, diagnosis and treatment of EML4-ALK NSCLC.. \"'), ('9595', 'TGFB_SMAD2', '', 'TGFB', 'SMAD2', '16914899', '10', '', '', '', '', 'Tumor_suppressor', '', 'Transcription_Factor', '', '', ' Smad2 is an important factor in TGFbeta/Smad2 signal transduction pathway with ability for signal propagation, it could translocate from cytoplasm to nucleus after the TGFbeta receptor-mediated phosphorylation.     ///    \"However, no quantification data have been yet reported, and it still keeps suspenseful whether or not 15d-PGJ2 could regulate Smad2 activity by depending on PPARgamma through PPAR gamma/TGFbeta/ Smad2 pathway. \"'), ('9596', 'PDK1_AKT1', '', 'PDK1', 'AKT1', '19844585', '10', '', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'At high H(2)O(2), Akt1-PDK1 association is disrupted and P-Akt1 Ser(473) accumulates in mitochondria in detriment to nuclear translocation. '), ('9597', 'IL8_COX2', '', 'IL8', 'COX2', '21777689', '10', '', '', '', '', '', '', '', '', '', 'During this process, the increased levels of COX-2/IL-8 and the subsequent elevation of ROS production induced NF-?B nuclear translocation and IL-8 secretion.     ///    Blockade of tropomyosin receptor kinase A (TrkA) by an inhibitor or short hairpin RNA inhibited the levels of COX-2/IL-8 and the nuclear translocation of NF-?B but did not suppress the increased ROS level. '), ('9598', 'PDCD1LG2_JAK2', '', 'PDCD1LG2', 'JAK2', '18940474', '10', 'Hodgkin lymphoma', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'To identify the translocation partners, these cases were further studied with probes for the MYC, BCL2, BCL6, BCL3, REL/BCL11A, JAK2/PDCD1LG2 (alias PDL2) C14orf43, and C2TA loci. '), ('9599', 'SYT_SSX1', '', 'SYT', 'SSX1', '24436244', '10', 'synovial sarcoma;small cell carcinoma;squamous cell carcinoma;sarcoma\r\r', '', '', '', '', '', '', '', '', '18) SYT/SSX1 translocation confirming the diagnosis of SS. '), ('9600', 'HSA_AGE', '', 'HSA', 'AGE', '19645720', '10', '', '', '', '', '', '', '', '', '', 'Similar to lipopolysaccharide, AGE-HSA stimulation induced mitogen-activated protein kinase phosphorylation and nuclear factor-kappaB nuclear translocation in human umbilical vein endothelial cells, which was further enhanced by a combination of the two stimulants.     ///    \"Pharmacological inhibitions of each individual signaling pathway, including p38, extracellular signal-regulated kinase 1/2, Jun N-terminal kinase and nuclear factor-kappaB, revealed that activation of all of these four pathways is necessary for the effective induction of interleukin-6, interleukin-8 and monochemoattractant protein-1 by both AGE-HSA and lipopolysaccharide. \"'), ('9601', 'XIAP_GSN', '', 'XIAP', 'GSN', '24771612', '10', 'head and neck cancer', '', '', '', '', '', '', '', '', 'In chemosensitive cells, cisplatin suppressed GSN-XIAP interaction, promoted translocation of XIAP from the perinuclear region to the nucleus and induced apoptosis.     ///    \"In chemoresistant cells, GSN was highly expressed, and cisplatin had no significant effect on GSN-XIAP interaction and apoptosis. \"'), ('9602', 'P65_NFKB1', '', 'P65', 'NFKB1', '15791843', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'It is concluded that degradation of IkappaB-alpha protein and NF-kappaB/p65 translocation occur during TNF-alpha-induced apoptosis of U937 cells, suggesting the activation of NF-kappaB TPCK-sensitive protease plays an important role in the degradation of IkappaB-alpha protein induced by TNF-alpha in U937 cells.     ///    \"Immunolfluorescence assay showed that NF-kappaB/p65, IkappaB-alpha only localized in cytoplasm. \"    ///    \" To investigate the effect of N-tosyl-L-phenylalanylchloromethyl ketone (TPCK) on tumor necrosis factor-alpha-induced NF-kappaB activation and apoptosis in U937 cell line, changes and subcellular localization of NF-kappaB/p65 and IkappaB-alpha were observed by fluorescencemicroscopy and expression and degradation of IkappaB-alpha by flow cytometry. \"'), ('9603', 'P65_NFKB1', '', 'P65', 'NFKB1', '15336524', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'Both analysis by immunocytochemistry and of immunoblots revealed that NF-kappaB-p65 was translocated into the nuclei following 6-OHDA but not MPP(+)-treatment.     ///    A competition assay indicated that not only NF-kappaB-p65 but also -p50 is involved in 6-OHDA-induced NF-kappaB activity. '), ('9604', 'P65_NFKB1', '', 'P65', 'NFKB1', '17031850', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'HNE abrogated IL-1beta-induced iNOS expression and promoter activity mainly through NF-kappaB site (-5,817/-5,808) possibly via suppression of IKKalpha-induced IkappaBalpha phosphorylation and NF-kappaB/p65 nuclear translocation. '), ('9605', 'MAPK3_P42', '', 'MAPK3', 'P42', '15784655', '10', '', '', 'Kinase', '', '', '', '', '', '', 'YC-1 inhibited VEGF- and bFGF-induced p42/p44 mitogen-activated protein kinase and Akt phosphorylation as well as protein kinase C alpha translocation using Western blot analysis. '), ('9606', 'HER3_HER2', '', 'HER3', 'HER2', '25398453', '10', 'breast cancer', 'FISH;PCR;RT-PCR ', '', '', '', '', '', '', '', 'The possible role of high HER2:HER3 heterodimers in predicting response to lapatinib merits investigation in HER2(-) tumors.. '), ('9607', 'MALT1_API2', '', 'MALT1', 'API2', '17085907', '10', 'gastric cancer', '', '', '', '', '', '', '', '', 'pylori and t (11;18) (q21;q21) translocation (API2-MALT1 gene). '), ('9608', 'PAH_HMW', '', 'PAH', 'HMW', '17706349', '10', '', '', '', '', '', '', '', '', '', 'Linear regression analyses showed that the relationships between soil and shoot PAH concentrations were stronger for LMW-PAHs (R(2) between 0.51 and 0.92) than for HMW-PAHs (R(2) 0.02 and 0.60), suggesting that translocation for LMW-PAHs is faster than HMW-PAHs.     ///    \"Furthermore, the data imply that root uptake was the main pathway for HMW-PAHs accumulation. \"'), ('9609', 'TRNQ_TRNI', '', 'TRNQ', 'TRNI', '22978261', '10', '', '', '', '', '', '', '', '', '', 'All genes are arranged in their conserved positions compared with the pupative ancestral arrangement of insects except for trnM, which was translocated to the upstream of the transfer RNA cluster trnI-trnQ as in all previously reported lepidopteran mitochondiral genomes. '), ('9610', 'MYC_IGH', '', 'MYC', 'IGH', '17639584', '10', 'B cell lymphoma;lymphoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'In a model of immunoglobulin heavy-chain (IGH)/MYC translocation, the Igh 3\' regulatory region induces MYC expression at the immature stage of B cell development.. '), ('9611', 'gastrin_CCK', '', 'gastrin', 'CCK', '2884163', '10', '', '', '', '', '', '', '', '', '', 'auratus 10 endocrine cell types can be distinguished: neurotensin-, secretin-, serotonin-, somatostatin-, and two types of substance P-immunoreactive cells exclusively in the stomach, and C-t-gastrin/CCK-, glucagon-, Met-enkephalin-, PP-, and only one type of substance P-immunoreactive cells in the intestinal epithelium. '), ('9612', 'MSH2_MLH1', '', 'MSH2', 'MLH1', '16394087', '10', 'multiple endocrine neoplasia', 'PCR', '', '', '', '', '', '', '', 'MMR was assessed by MLH1/MSH2 sequencing and immunostaining in pheochromocytomas with two or more abnormal microsatellites.     ///    \"No mutations were identified in MLH1/MSH2, but MMR proteins significantly decreased in peripheral compartments. \"'), ('9613', 'P65_P50', '', 'P65', 'P50', '25627693', '10', '', '', '', '', '', '', '', '', '', 'NF2 was not able to stimulate RAW264.7 cells to release NO without its protein moiety, which was essential to activate NF-?B pathway through the degradation and phosphorylation of I?B-? and the subsequent translocation of p65/p50 complex in the cell nucleus. '), ('9614', 'CFL1_ADF', '', 'CFL1', 'ADF', '22139132', '10', '', '', '', '', '', '', '', '', '', 'ADF/cofilin proteins translocate to mitochondria during apoptosis but are not generally required for cell death signaling..     ///    \"Thus, we conclude that ADF/cofilin activity is not generally required for induction or progression of apoptosis in mammalian cells. \"    ///     Non-muscle cofilin (n-cofilin) is a member of the ADF/cofilin family of actin depolymerizing proteins.     ///    \"To elucidate the general importance of ADF/cofilin activity for apoptosis, we exposed mouse embryonic fibroblasts deficient for n-cofilin, ADF (actin depolymerizing factor), or all ADF/cofilin isoforms to well-characterized apoptosis inducers. \"'), ('9615', 'P35_CDK5', '', 'P35', 'CDK5', '17506859', '10', '', '', 'Kinase', '', '', '', '', '', '', 'p25 translocated to the nucleus in ER-stressed neurons, whereas p35/Cdk5 was perinuclear in control neurons. '), ('9616', 'SYT_SSX2', '', 'SYT', 'SSX2', '17130329', '10', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Diagnosis was confirmed with SYT-SSX2 translocation detection.. '), ('9617', 'ICAD_CAD', '', 'ICAD', 'CAD', '10908575', '10', '', '', 'Kinase', '', '', '', '', '', '', 'It was initially proposed that proteolytic cleavage of ICAD by activated caspases causes the dissociation of the ICAD/CAD heterodimer and the translocation of active CAD into the nucleus in apoptotic cells.     ///    \"The two NLSs have an additive effect on the nuclear targeting of the CAD-ICAD complex, whereas ICAD-S, lacking its NLS, appears to have a modulatory role in the nuclear localization of CAD. \"    ///    Determinants of the nuclear localization of the heterodimeric DNA fragmentation factor (ICAD/CAD)..     ///    \"We conclude that a complex mechanism, involving the recognition of the NLSs of both ICAD and CAD, accounts for the constitutive accumulation of CAD/ICAD in the nucleus, where caspase-3-dependent regulation of CAD activity takes place.. \"'), ('9618', 'DUX4_CIC', '', 'DUX4', 'CIC', '24980961', '10', 'ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Unusual primary cerebral localization of a CIC-DUX4 translocation tumor of the Ewing sarcoma family.. '), ('9619', 'P65_P50', '', 'P65', 'P50', '15845480', '10', 'pneumonia', '', '', '', '', '', '', '', '', 'These data were confirmed in gel shift assays, providing direct evidence that Pneumocystis induced the nuclear translocation of the p50/p65 heterodimeric form of NF-kappaB. '), ('9620', 'BCR_ABL1', '', 'BCR', 'ABL1', '20442364', '10', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia;down syndrome\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'We reviewed data from 2811 children with ALL enrolled in Children\'s Oncology Group P9900, which included prospective testing for the major cytogenetic lesions in childhood ALL: ETV6-RUNX1, TCF3-PBX1, BCR-ABL1, and MLL translocations and trisomies of chromosomes 4 and 10.     ///    \"However, when children with MLL translocations, BCR-ABL1, ETV6-RUNX1, and trisomies 4 and 10 were excluded, the EFS and OS were similar for children with and without DS (EFS 68.0 %+/- 9.3% vs 70.5% +/- 1.9%, P = .817. \"'), ('9621', 'PRX1_NES', '', 'PRX1', 'NES', '17603937', '10', '', '', '', '', '', '', '', '', '', 'Results showed that NES-Prx1 inhibited NF-kappaB activation and nuclear translocation.     ///    \"Interestingly, following treatment with H(2)O(2), nuclear thioredoxin-1 (Trx1) redox status was protected by NLS-Prx1, and cytoplasmic Trx1 was protected by NES-Prx1. \"    ///    \"Both NLS-Prx1 and NES-Prx1 inhibited NF-kappaB p50 oxidation, suggesting that oxidation of the redox-sensitive cysteine in p50\'s DNA-binding domain is regulated via peroxide metabolism in both compartments. \"'), ('9622', 'EML4_ALK', '', 'EML4', 'ALK', '22196919', '10', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'A major contributor has been the discovery of molecular subtypes harbouring a critical oncogenic driver mutation, specifically sensitizing mutations in the epidermal growth factor receptor (EGFR) gene and the EML4-ALK gene translocation. '), ('9623', 'MMSET_FGFR3', '', 'MMSET', 'FGFR3', '23288641', '10', 'multiple myeloma\r\r', '', 'Kinase', '', '', '', '', '', '', 'Commonly detected genetic aberrations are translocations involving immunoglobulin heavy chain (IgH) switch regions (chromosome 14q32) and oncogenes such as c-maf [t(14:16)], cyclin D1 [t(11:14)], and FGFR3/MMSET [t(4:14)]. '), ('9624', 'MDM2_GSTP5', '', 'MDM2', 'GSTP5', '27038437', '10', '', '', '', 'Oncogene', '', '', '', '', '', 'Although the translocation of positively charged MDM2 through a nanopore was detected at the applied negative voltage, this MDM2 translocation was almost completely blocked upon formation of the MDM2/GST-p53TAD complex owing to charge conversion.     ///    \"In combination with NMR data, the nanopore measurements showed that the addition of Nutlin-3 rescued MDM2 translocation, indicating that Nutlin-3 disrupted the MDM2/GST-p53TAD complex, thereby releasing MDM2. \"'), ('9625', 'PAX3_FKHR', '', 'PAX3', 'FKHR', '19295433', '10', 'rhabdomyosarcoma;renal cell carcinoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'The pathway from PAX3-FKHR translocation to the development of rhabdomyosarcoma tumors has been further elucidated. '), ('9626', 'PGD_IVF', '', 'PGD', 'IVF', '22161460', '10', '', '', '', '', '', '', '', '', '', 'Until a well-designed study comparing the two strategies is performed, or at least prospective cohort studies with strict entry criteria and definitions, the cumulative experience and success of both medical management and IVF/PGD must be used to counsel patients who are carriers of a reciprocal translocation, ascertained on the basis of recurrent pregnancy loss..     ///    \"Based on this systematic review, successful pregnancy outcomes are high following either medical management or IVF/PGD for carriers of a reciprocal translocation, ascertained on the basis of recurrent pregnancy loss. \"    ///    Cumulative live birthrate was 74% (81 of 109 cases) in the medical management group and 35% (7 of 20) in the IVF/PGD group.     ///    Subsequent pregnancy outcomes were tabulated based on whether management was medical or involved in vitro fertilization/preimplantation genetic diagnosis (IVF/PGD).     ///    Management was medical in 109 cases and IVF/PGD in 20 cases. '), ('9627', 'RAC1_CDC42', '', 'RAC1', 'CDC42', '14557270', '10', '', '', '', '', '', '', '', '', '', '277, 44417-44430) we reported that phosphorylation of p85 betaPIX, a guanine nucleotide exchange factor (GEF) for Rac1/Cdc42, is a signal for translocation of the PIX complex to neuronal growth cones and is associated with basic fibroblast growth factor (bFGF)-induced neurite outgrowth.     ///    \"However, the issue of whether p85 betaPIX phosphorylation affects GEF activity on Rac1/Cdc42 is yet to be explored. \"'), ('9628', 'PGD_IVF', '', 'PGD', 'IVF', '15866591', '10', 'ovarian hyperstimulation syndrome', '', '', '', '', '', '', '', '', 'In couples undergoing IVF/PGD to avoid transmission of an unbalanced karyotype, a significantly higher proportion of women carrying balanced translocations (female carrier) responded very poorly (E2 on the day of hCG <1,000 pg/mL) to ovarian stimulation compared to women whose partner had a balanced translocation (male carrier) (23.0% vs.     ///    \"In couples undergoing IVF/PGD for balanced translocation, the risk for poor response to ovarian stimulation may be increased when the female partner carries the balanced translocation compared to when the male partner carries the translocation. \"'), ('9629', 'TFIID_ATF4', '', 'TFIID', 'ATF4', '23332750', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'DNA labeling and footprinting, together with cryo-EM studies, were used to map the locations of TATA, Initiator (Inr), motif ten element (MTE), and downstream core promoter element (DPE) promoter motifs within the TFIID-TFIIA-DNA structure. '), ('9630', 'MAPK3_P42', '', 'MAPK3', 'P42', '14751540', '10', '', '', 'Kinase', '', '', '', '', '', '', 'BK also stimulated translocation of p42/p44 MAPK into nucleus and led to expression of c-fos and c-jun in CKs.     ///    BK stimulated [3H]thymidine incorporation and p42/p44 MAPK phosphorylation in a time- and concentration-dependent manner.     ///    \"These results demonstrate that in CKs, BK-stimulated phosphorylation of p42/p44 MAPK is mediated through the activation of BK B2 receptors and leads to cell proliferation.. \"    ///    Bradykinin-stimulated p42/p44 MAPK activation associated with cell proliferation in corneal keratocytes..     ///    \"This study was to investigate the mitogenic effect of BK on rabbit CKs linked to activation of p42/p44 mitogen-activated protein kinase (MAPK), assessed by [3H]thymidine incorporation and Western blotting analysis, respectively. \"'), ('9631', 'P65_NRF1', '', 'P65', 'NRF1', '24466341', '10', 'prostate cancer\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'DHT-induced AR transactivation was coupled with higher nuclear translocation of p65-Nrf1 in C4-2B cells, as compared to LNCaP cells.     ///    \"Quantitative RT-PCR studies further validated the inductive effects of p65-Nrf1 isoform on the androgen regulated genes, PSA and TMPRSS2. \"    ///    \"Subsequent studies showed that Nrf1 physically interacts with AR and enhances AR\'s DNA-binding activity, suggesting that the p65-Nrf1 isoform is a potential AR coactivator. \"    ///    \"Interestingly, siRNA mediated silencing of Nrf1 attenuated AR transactivation while p65-Nrf1 overexpression enhanced AR transactivation. \"    ///    Our findings also indicate that the DHT-stimulated increase in p65-Nrf1 and the simultaneous suppression of both Nrf2 and p120-Nrf1 ultimately facilitates AR transactivation in CRPC cells. '), ('9632', 'P65_P50', '', 'P65', 'P50', '23727177', '10', '', '', '', '', '', '', '', '', '', 'Molecular studies showed that BISA suppressed MAPK phosphorylation and nuclear translocation of NF-?B p50/p65. '), ('9633', 'WAF1_CIP1', '', 'WAF1', 'CIP1', '12370305', '10', '', '', '', '', '', '', '', '', '', 'We demonstrated that in PMA-induced adherent cells, upregulation of p21(Cip1/Waf1) requires the activation and nuclear translocation of phosphorylated extracellular signal-regulated kinase (phospho-ERK).     ///    Cytosolic retention of phosphorylated extracellular signal-regulated kinase and a Rho-associated kinase-mediated signal impair expression of p21(Cip1/Waf1) in phorbol 12-myristate-13- acetate-induced apoptotic cells..     ///    Expression of the cell cycle inhibitor p21(Cip1/Waf1) was induced after PMA treatment in the adherent cells but not in the proapoptotic cells.     ///    \"Finally, we demonstrated that inhibition of ROCK restores nuclear distribution of phospho-ERK and activation of p21(Cip1/Waf1) expression. \"    ///    \"Based on these findings, we propose that a ROCK-mediated signal is involved in interfering with the process of ERK-mediated p21(Cip1/Waf1) induction in PMA-induced proapoptotic TF-1 and D2 cells.. \"    ///    \"We also found that only PMA-induced proapoptotic cells contained the phosphorylated form of myosin light chain, which is dependent on Rho-associated kinase (ROCK) activation, and that expression of a dominant-active form of ROCK suppressed activation of the p21(Cip1/Waf1) promoter during PMA induction. \"    ///    We investigated the mechanism responsible for the impairment of p21(Cip1/Waf1) induction in PMA-induced proapoptotic cells. '), ('9634', 'FUS_ATF1', '', 'FUS', 'ATF1', '23320232', '10', 'melanoma;fibrous histiocytoma;histiocytoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', 'Seq', 'So far three translocations have been reported to arise in angiomatoid fibrous histiocytoma: FUS-ATF1, EWSR1-CREB1, or EWSR1-ATF1. '), ('9635', 'NPM_ALK', '', 'NPM', 'ALK', '21703420', '10', 'anaplastic large cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'Finally, NPM-ALK impeded the expected DNA damage-induced translocation of MSH2 out of the cytoplasm.     ///    \"Using co-immunoprecipitation, we found that increasing levels of NPM-ALK expression in HEK293 cells resulted in decreased levels of MSH6 bound to MSH2, whereas MSH2??NPM-ALK binding was increased. \"    ///    MSH2 was found to be tyrosine phosphorylated in the presence of NPM-ALK.     ///    \"In this study, we found in vitro evidence that enforced expression of NPM-ALK in HEK293 cells suppressed MMR function. \"    ///    \"To conclude, our data support a model in which the suppression of MMR by NPM-ALK is attributed to its ability to interfere with normal MSH2 biochemistry and function.. \"    ///    Fusion tyrosine kinase NPM-ALK Deregulates MSH2 and suppresses DNA mismatch repair function novel insights into a potent oncoprotein..     ///     The fusion tyrosine kinase NPM-ALK is central to the pathogenesis of ALK-positive anaplastic large cell lymphoma (ALK(+)ALCL). '), ('9636', 'STIM1_ORAI1', '', 'STIM1', 'ORAI1', '18542992', '10', '', '', '', '', '', '', '', '', '', 'We can therefore conclude that STIM1 translocation and re-translocation as well as formation of STIM1-ORAI1 clusters occur in an ATP-independent fashion and under conditions of PI(4,5)P(2) depletion..     ///    ATP depletion induces translocation of STIM1 to puncta and formation of STIM1-ORAI1 clusters: translocation and re-translocation of STIM1 does not require ATP..     ///    STIM1-ORAI1 clusters that developed as a result of ATP depletion were very poor mediators of Ca(2+) influx. '), ('9637', 'TEL_AML1', '', 'TEL', 'AML1', '12613515', '10', 'leukemia\r\r', 'PCR', '', '', '', '', '', '', '', ' We established a real-time PCR method that can simultaneously detect 10 different fusion transcripts (major, minor and micro BCR/ABL, AML1/MTG8, PML/RARalpha, CBFbeta/MYH11, TEL/AML1, E2A/PBX1, MLL/AF4, and MLL/AF9) together with Wilms\' tumor gene (WT1) transcripts. '), ('9638', 'P65_NFKB1', '', 'P65', 'NFKB1', '11770011', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'Western blotting of nuclear extracts of A549 cells demonstrated that theophylline suppresses NF-kappaB-p65 nuclear translocation. '), ('9639', 'YPEL5_PPP1CB', '', 'YPEL5', 'PPP1CB', '23382248', '10', 'chronic lymphocytic leukemia;leukemia\r\r', 'PCR', '', '', '', '', '', '', '', 'Using quantitative real-time PCR (q real-time PCR), YPEL5/PPP1CB and PPP1CB/YPEL5 fusion transcripts were detected in 97 of 103 CLL samples (95%) but not in paired normal samples, benign lymphocytes, or various unrelated cancers.     ///    \"YPEL5/PPP1CB chimera, when introduced into mammalian cells, expressed a truncated PPP1CB protein that demonstrated diminished phosphatase activity. \"'), ('9640', 'STIM1_ORAI1', '', 'STIM1', 'ORAI1', '25517631', '10', '', '', '', '', '', '', '', '', '', 'Notably, store depletion results in transient localization of STIM1-Orai1 in the PI(4,5)P2-poor microdomain, which then translocates to the PI(4,5)P2-rich domain.     ///     The Orai1-STIM1 current undergoes slow Ca(2+)-dependent inactivation (SCDI) mediated by the binding of SARAF to STIM1.     ///    \"Targeting STIM1 to PI(4,5)P2-rich and -poor microdomains reveals that SARAF-dependent SCDI is observed only when STIM1-Orai1 are within the PI(4,5)P2-rich microdomain. \"    ///    Here we report the use of SCDI by SARAF as a probe of the conformation and microdomain localization of the Orai1-STIM1 complex.     ///    \"STIM1-Orai1 must be in a PM/ER microdomain tethered by E-Syt1, stabilized by septin4 and enriched in PI(4,5)P2 for STIM1-SARAF interaction. \"'), ('9641', 'P43_P41', '', 'P43', 'P41', '25228008', '10', 'non small cell lung cancer;lung cancer\r\r', '', '', '', '', '', '', '', '', 'Moreover, we found that cytoplasmic p27 bound to a cleaved intermediate (p43/p41) of caspase 8 and that inhibition of cytoplasmic translocation of p27 reduced gefitinib-induced cell death in HCC827 cells. '), ('9642', 'SYK_ITK', '', 'SYK', 'ITK', '24076779', '10', 'T cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'ITK/SYK translocation in angioimmunoblastic T-cell lymphoma.. '), ('9643', 'CD69_CD40', '', 'CD69', 'CD40', '15879108', '10', '', '', '', '', '', '', '', '', '', 'Interestingly, DOTAP-mediated enhanced endosomal translocation of otherwise nonstimulatory vertebrate DNA or of certain noncanonical CpG motifs triggers robust dendritic cell activation in terms of both up-regulation of CD40/CD69 and cytokine production, such as type I IFN and IL-6. '), ('9644', 'SYT_SSX1', '', 'SYT', 'SSX1', '21454665', '10', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Synovial sarcoma is an aggressive soft tissue tumor characterized by a chromosomal translocation between chromosome 18 and X, generating oncoproteins such as SYT-SSX1 and SYT-SSX2.     ///    SYT-SSX1 (synovial sarcoma translocated) regulates PIASy ligase activity to cause overexpression of NCOA3 protein..     ///    \"Here we show that SYT-SSX1 leads to up-regulation of NCOA3, a protein critical for the formation of various cancers. \"    ///    The molecular mechanism underlying the oncogenic potential of SYT-SSX1/2 is not clear.     ///    \"SYT-SSX1 does so by increasing the sumoylation of NCOA3 through interaction with a SUMO E3 ligase, PIASy, as well as the sumoylation of NEMO. \"'), ('9645', 'P65_P50', '', 'P65', 'P50', '23437404', '10', 'prostate cancer\r\r', '', '', '', '', '', '', '', '', 'In the present study we show that suppression of NF-?B activation by ?-tomatine occurs through inhibition of I kappa B alpha (I?B?) kinase activity, leading to sequential suppression of I?B? phosphorylation, I?B? degradation, NF-?B/p65 phosphorylation, and NF-?B p50/p65 nuclear translocation. '), ('9646', 'MUM1_IRF4', '', 'MUM1', 'IRF4', '21659362', '10', 'follicular lymphoma;B cell lymphoma;lymphoma\r\r', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', '', '', 'Both follicular lymphoma grade 3B and diffuse large B-cell lymphoma/follicular lymphoma grade 3B were enriched in samples with a CD10(-)IRF4/MUM1(+) immunophenotype (8/19, 42% and 7/16, 44%), with the vast majority of them lacking BCL2 translocations.     ///    \"We performed a detailed immunohistochemical (CD10, IRF4/MUM1, BCL2, Ig light chains) and genetic (translocations of BCL2, BCL6, MYC, IRF4) characterization of the largest series of purely follicular cases of grade 3B follicular lymphoma available to date, comprising 23 tumor samples. \"    ///    \"Our results show that grade 3B follicular lymphomas form a distinct category of follicular lymphomas with infrequent BCL2 and BCL6 translocations, while grades 1, 2 and 3A follicular lymphomas and FL/LCC display homogeneous features with frequent BCL2 translocations and a CD10(+)IRF4/MUM1(-) immunophenotype.. \"    ///    None of the tumor samples tested with increased IRF4/MUM1-expression harbored a translocation of the IRF4 gene locus.     ///    \"In contrast, 42/46 grade 1 or 2 follicular lymphomas, FL/LCC and grade 3A follicular lymphomas were CD10(+) (91%) while 0/46 expressed IRF4/MUM1. \"'), ('9647', 'TRKC_TEL', '', 'TRKC', 'TEL', '12024032', '10', 'non Hodgkin lymphoma;leukemia;lymphoma\r\r', '', '', '', '', '', '', '', '', ' Fusion tyrosine kinases (FTKs) such as BCR/ABL, TEL/ABL, TEL/JAK2, TEL/PDGF beta R, TEL/TRKC(L), and NPM/ALK arise from reciprocal chromosomal translocations and cause acute and chronic leukemias and non-Hodgkin\'s lymphoma.     ///    \"Various FTKs, except TEL/TRKC(L), can activate STAT5, which may be required to induce drug resistance. \"'), ('9648', 'NRF2_KEAP1', '', 'NRF2', 'KEAP1', '24116287', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'The biochemical mechanisms underlying the phosphorylation and expression of Keap1/Nrf2 proteins that are controlled by the intracellular signaling kinases and ubiquitin-mediated E3 ligase system as well as control of nucleocytoplasmic translocation of Nrf2 by its innate nuclear export signal (NES) are described.     ///    \"In the present review, the functional significance of Keap1/Nrf2 protein module in regulating ARE-dependent phase II detoxification and anti-oxidant gene expression is discussed. \"'), ('9649', 'NUP98_HOXD13', '', 'NUP98', 'HOXD13', '24449168', '10', 'acute myeloid leukemia;myeloid leukemia;myelodysplastic syndrome;leukemia\r\r', '', '', 'Oncogene', '', '', '', 'KB', 'Seq', 'This study examines the collaboration of the loss of p15Ink4b with Nup98-HoxD13 translocation in the development of hematological malignancies in a mouse model.     ///    \"Here, we report that loss of p15Ink4b collaborates with Nup98-HoxD13 transgene in the development of predominantly myeloid neoplasms, namely acute myeloid leukemia, myeloproliferative disease, and myelodysplastic syndromes. \"    ///    Brief report: Loss of p15Ink4b accelerates development of myeloid neoplasms in Nup98-HoxD13 transgenic mice.. '), ('9650', 'FLI1_EWSR1', '', 'FLI1', 'EWSR1', '22460902', '10', 'ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', 'Seq', 'Unexpected relationships were revealed, including the marked sensitivity of Ewing\'s sarcoma cells harbouring the EWS (also known as EWSR1)-FLI1 gene translocation to poly(ADP-ribose) polymerase (PARP) inhibitors. '), ('9651', 'MYC_IGK', '', 'MYC', 'IGK', '19535347', '10', 'B cell lymphoma;leukemia', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'Overall survival was not different between the MYC-IGH translocation group (n=14) and the MYC-IGK or MYC-IGL translocation group (n=13).     ///    \"The MIB-1 index was investigated in 14 cases with aggressive B-cell lymphoma, and was higher in the group with MYC-IGH translocation (n=7) than in the MYC-IGK/L group (n=7) (p=0.02). \"'), ('9652', 'RXRA_NUR77', '', 'RXRA', 'NUR77', '15731112', '10', '', '', '', '', '', 'Receptor', 'Transcription_Factor', '', '', 'Rapid apoptosis induction by IGFBP-3 involves an insulin-like growth factor-independent nucleomitochondrial translocation of RXRalpha/Nur77.. '), ('9653', 'TNFA_IL1B', '', 'TNFA', 'IL1B', '16920886', '10', 'cystic fibrosis', '', '', '', '', '', '', '', '', 'Continuous inhibition of CFTR-Cl(-) conductance for 3-5 days resulted in significant increase in IL-8 secretion at basal (P = 0.006) and in response to 10(9) Pseudomonas (P = 0.0001), a fourfold decrease in Smad3 expression (P = 0.02), a threefold increase in RhoA expression, and increased NF-kappaB nuclear translocation upon TNF-alpha/IL-1beta stimulation (P < 0.000001). '), ('9654', 'SLIT2_ROBO1', '', 'SLIT2', 'ROBO1', '22826604', '10', 'breast cancer\r\r', '', '', '', '', '', '', '', '', 'The presence of an active Slit2/Robo1 signal blocks the translocation of ?-catenin into nucleus, leading to downregulation of c-myc and cyclin D1 via the phosphoinositide 3-kinase (PI3K)/Akt pathway. '), ('9655', 'YWHAE_FAM', '', 'YWHAE', 'FAM', '25130488', '10', 'sarcoma\r\r', '', '', '', '', '', '', '', '', 'All tumors were evaluated for the presence of a YWHAE-FAM translocation. '), ('9656', 'TEL_AML1', '', 'TEL', 'AML1', '24632701', '10', 'acute lymphoblastic leukemia;T ALL;lymphoblastic leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'TEL/AML1 translocation was detected in 28% of patients. '), ('9657', 'TNFA_ATA', '', 'TNFA', 'ATA', '14599555', '10', '', '', '', '', '', '', '', '', '', 'Reversal of TNF-alpha/ATA effects occurred in the presence of the PI-3K specific inhibitors wortmannin or LY294002 in the culture medium and was coincident with inhibition of the translocation of PKCzeta in the nucleus, while NF-kappaB was less affected. '), ('9658', 'RARA_PML', '', 'RARA', 'PML', '23320012', '10', 'acute promyelocytic leukemia;leukemia\r\r', '', '', 'Oncogene', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'Molecular methods for genomic analyses of variant PML-RARA or other RARA-related chromosomal translocations in acute promyelocytic leukemia.. '), ('9659', 'MAPK3_P42', '', 'MAPK3', 'P42', '15953648', '10', '', '', 'Kinase', '', '', '', '', '', '', 'Intracellular translocation of the decapeptide carboxyl terminal of Gi3 alpha induces the dual phosphorylation of p42/p44 MAP kinases.. '), ('9660', 'SHP2_ERK', '', 'SHP2', 'ERK', '20348091', '10', 'gastric cancer\r\r', '', '', '', '', '', '', '', '', 'In this study, we evaluated the effect of translocated CagA in relation to its tyrosine phosphorylation status on the gp130-mediated signal switch between the SHP2/ERK and JAK/STAT3 pathways.     ///    Disruption of the gp130 receptor that modulates the balance of the SHP2/ERK and JAK/STAT pathways enhanced peptic ulceration and gastric cancer in gp130 knock-out mice.     ///    \"These findings indicate that the phosphorylation status of CagA affects the signal switch between the SHP2/ERK and JAK/STAT3 pathways through gp130, providing a novel mechanism to explain H. \"    ///    Helicobacter pylori CagA phosphorylation status determines the gp130-activated SHP2/ERK and JAK/STAT signal transduction pathways in gastric epithelial cells.. '), ('9661', 'P65_P50', '', 'P65', 'P50', '16112027', '10', '', '', '', '', '', '', '', '', '', 'When CM, NES2Y, and primary islet cells were transfected by AdIkappaB(SA)2, TRAIL-induced IkappaB degradation and nuclear translocation of NF-kappaB p50/p65 were blocked. '), ('9662', 'EML4_ALK', '', 'EML4', 'ALK', '22614968', '10', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'gefitinib, erlotinib, and cetuximab for the treatment of NSCLC harboring epidermal growth factor receptor mutation or overexpression, and crizotinib for the treatment of NSCLC with the EML4-ALK fusion translocation oncogene being some examples. '), ('9663', 'FASL_FAS', '', 'FASL', 'FAS', '26578299', '10', '', '', '', '', '', '', '', '', '', 'Furthermore, pretreatment with isorhamnetin specifically inhibited FAS/FASL expression and suppressed nuclear factor-kappa B nuclear translocation. '), ('9664', 'SLC34A2_ROS1', '', 'SLC34A2', 'ROS1', '22617245', '10', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The SLC34A2-ROS1 translocated HCC78 cell line had phosphorylated levels of ROS1, AKT, and ERK inhibited by submicromolar doses of crizotinib, and subsequently underwent apoptosis.     ///    \"We selected NSCLC cell lines--A549 (KRAS G12S), NCI-H3255 (EGFR L858R), NCI-H3122 (EML4-ALK E13;A20), and HCC78 (SLC34A2-ROS1)-to evaluate the antiproliferative effects of submicromolar concentrations of the multitargeted TKIs imatinib, sorafenib, erlotinib, and crizotinib. \"'), ('9665', 'RAD51_BRCA2', '', 'RAD51', 'BRCA2', '21400509', '10', '', '', '', '', 'Tumor_suppressor', '', '', '', '', 'Mechanistically, we show that MET inhibition affects the formation of the RAD51-BRCA2 complex, which is crucial for error-free HR repair of double strand DNA lesions, presumably via downregulation and impaired translocation of RAD51 into the nucleus. '), ('9666', 'BCL2_ASPP2', '', 'BCL2', 'ASPP2', '25032846', '10', 'hepatocellular carcinoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'Although the role of nuclear ASPP2-Bcl-2 complexes is still unclear, our results suggest that nuclear ASPP2 can prevent the translocation of the remaining Bcl-2 to the cytoplasm by binding to Bcl-2 in a CHOP-dependent manner, and this effect also contributes to Beclin-1-initiated autophagy.     ///    \"Thus, CHOP is critical for mediating ASPP2-induced autophagic apoptosis by decreasing Bcl-2 expression and maintaining nuclear ASPP2-Bcl-2 complexes. \"'), ('9667', 'MEK_ERK', '', 'MEK', 'ERK', '15239952', '10', '', '', '', '', '', '', '', '', '', 'Thus, hSef binds to activated forms of MEK, inhibits the dissociation of the MEK-ERK complex, and blocks nuclear translocation of activated ERK. '), ('9668', 'CCND1_CDK4', '', 'CCND1', 'CDK4', '16293976', '10', '', 'PCR', 'Kinase', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'Disruptions at p16INK4A and/or cdk4/cyclin D1 concomitantly occurring with TP53 LOH may participate in the development of a subset of endometrioid-type ECs..     ///    \"p16INK4A alterations (LOH and gene deletion) occurred concomitantly, with 3 tumors showing the TP53 allelic loss, whereas the cyclin D1/cdk4 complex was overexpressed in a case with TP53 LOH. \"'), ('9669', 'EWSR1_ERG', '', 'EWSR1', 'ERG', '25441687', '10', 'ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'This is illustrated by a case previously thought to represent an atypical carcinoid tumor, in which an EWSR1-ERG translocation was detected during next generation sequencing using a hybrid capture approach, leading to a revised diagnosis of Ewing sarcoma. '), ('9670', 'ANG2_ANG1', '', 'ANG2', 'ANG1', '15498854', '10', '', '', '', '', '', '', '', '', '', 'Furthermore, combination of Ang1/Ang2 induced an additive effect on neutrophil adhesion but not on P-selectin translocation. '), ('9671', 'P65_P50', '', 'P65', 'P50', '25590437', '10', '', '', '', '', '', '', '', '', '', 'Cell free and in vivo studies demonstrate that RS induces phosphorylation of p50 in an ATR-dependent but DNA damage-independent manner that acts to modulate NF-?B activity without affecting p50/p65 nuclear translocation. '), ('9672', 'BIRC2_TRAF2', '', 'BIRC2', 'TRAF2', '15861135', '10', '', '', '', '', '', '', '', '', '', 'Furthermore, Ubc6 co-localized with translocated TRAF2/c-IAP1 in the ER-associated compartment in vivo, and a catalytically inactive Ubc6 mutant inhibited TNF-alpha-induced, TNF-R2-dependent TRAF2 degradation.     ///    TNF-alpha induced c-IAP1/TRAF2 complex translocation to a Ubc6-containing compartment and TRAF2 ubiquitination.. '), ('9673', 'MYC_Immunoglobulin ', '', 'MYC', 'Immunoglobulin ', '20197382', '10', 'lymphoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'Here, we report that elevated levels of Skp2 are a characteristic of Emu-Myc lymphomas and of human Burkitt lymphoma that bear MYC/Immunoglobulin chromosomal translocations. '), ('9674', 'S100C_A11', '', 'S100C', 'A11', '15205326', '10', 'hepatocellular carcinoma\r\r', '', '', '', '', '', '', '', '', 'S100C/A11 protein was translocated to and accumulated in nuclei of TGF-beta 1-treated JHH-5 cells, where p21/Waf1 was concomitantly accumulated.     ///    Involvement of interferon regulatory factor 1 and S100C/A11 in growth inhibition by transforming growth factor beta 1 in human hepatocellular carcinoma cells..     ///    Prior transfection of p21/Waf1-targeted small interfering RNA efficiently blocked decrease of DNA synthesis in JHH-5 cells caused by TAT-S100C/A11 or TGF-beta 1 and markedly inhibited expression of p21/Waf1 protein in the cells.     ///    \"Expression of S100C/A11, a member of the Ca(2+)-binding S100 protein family, also markedly increased after addition of TGF-beta 1. \"    ///    \"When a recombinant S100C/A11 protein was introduced into nuclei of JHH-5 cells, DNA synthesis was markedly inhibited in a dose-dependent manner in the absence of TGF-beta 1. \"    ///    These results indicate that IRF-1 and S100C/A11 mediate growth inhibition by TGF-beta 1 via induction of p21/Waf1.. '), ('9675', 'P65_P50', '', 'P65', 'P50', '26797421', '10', 'melanoma\r\r', '', '', '', '', '', '', '', '', 'In addition, silencing of MED27 led to the decrease of iNOS expression through inhibiting the activation of a serial of upstream key proteins of NF-?B signaling pathway and the translocation of p50/p65 from cytoplasm to nucleus. '), ('9676', 'RET_PTC1', '', 'RET', 'PTC1', '20369307', '10', 'thyroid carcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'Both tumors were analyzed for the BRAF (Val600Glu) mutation and the RET/PTC1 translocation.     ///    The PTC was positive for the BRAF mutation but negative for RET/PTC1. '), ('9677', 'NPRA_ANP', '', 'NPRA', 'ANP', '23526266', '10', '', '', '', '', '', '', '', '', '', 'The results of this study suggest that ANP/NPR-A signaling system antagonizes the agonist-induced collagen synthesis via suppressing the activities of MMP-2, MMP-9, ROS generation, and NF-?B nuclear translocation mechanism..     ///    \"Here, we investigated the anti-fibrotic mechanism of ANP/NPR-A in fibrotic agonist Angiotensin- II (ANG II)-treated adult cardiac fibroblast (CF) cells. \"    ///    \"However, the underlying mechanism by which ANP/NPR-A system opposes the ECM remodeling in the diseased heart is not well understood. \"'), ('9678', 'HMW_FGF2', '', 'HMW', 'FGF2', '26056081', '10', '', '', '', '', '', '', '', '', '', 'SiRNA-directed Kap?2 knockdown significantly reduced HMW-FGF2\'s nuclear translocation.     ///    Decreased PTEN expression and activated Akt signaling were observed upon HMW-FGF2 overexpression and might mediate pro-survival effect of FGF2.     ///    \"Nuclear accumulation of HMW-FGF2 strongly promotes glioblastoma cell proliferation, yet mechanism governing such cellular distribution remains unexplored. \"    ///    \"We found HMW-FGF2, but not 18K-FGF2, is primarily located in the nucleus and interacts with nuclear transport protein Karyopherin-?2/Transportin (Kap?2). \"    ///    \"Moreover, inhibiting Ran GTPase activity also resulted in decreased HMW-FGF2 nuclear accumulation. \"    ///    Proliferation of T98G cells is greatly enhanced with transfections HMW-FGF2. '), ('9679', 'TAL1_SIL', '', 'TAL1', 'SIL', '23317202', '10', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia\r\r', 'FISH;PCR;RT-PCR ', '', '', '', '', 'Transcription_Factor', '', '', 'RFS with BCR-ABL, MLL-AF4, TCF3-PBX1 and SIL-TAL1 was less than 10 months (8.0, 3.6, 5.5 and 8.1 months, respectively).     ///    11) and SIL-TAL1 (del 1p32) were found in 89/101 (88.1%) patients. '), ('9680', 'SMYD3_RIZ1', '', 'SMYD3', 'RIZ1', '24993551', '10', 'retinoblastoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'The SMYD3-RIZ1 pathway may represent a therapeutic target for esophageal squamous cell carcinoma. '), ('9681', 'ERK_EGFR', '', 'ERK', 'EGFR', '26805383', '10', '', 'PCR', 'Kinase', '', '', '', '', '', '', 'To understand the mechanism of the alteration of cell differentiation and proliferation, phosphorylation of signal molecules in EGFR/ERK pathway was investigated. '), ('9682', 'BCR_ABL1', '', 'BCR', 'ABL1', '8251912', '10', 'leukemia\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', ' Several important issues in CML research are not covered in this brief review such as the structural or molecular basis of the translocation between ABL and BCR, the relationship between CML and ALL with an identical or related BCR/ABL abnormality, the biology of CML stem and progenitor cells and immunologic aspects of CML. '), ('9683', 'ROS_NOX2', '', 'ROS', 'NOX2', '26359950', '10', '', 'PCR', '', '', '', '', '', '', '', 'S1P stimulated mTOR activation through the Nox2/ROS and PI3K/Akt pathways, which can further stimulate FoxO1 phosphorylation and translocation to the cytosol. '), ('9684', 'RET_PTC1', '', 'RET', 'PTC1', '16832789', '10', 'thyroid carcinoma;thyloid cancer;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'RET translocation in carcinoma type RET/PTC1 in elderly and RET/PTC3 in children, and expression Ax1 and Gas6 in children were reviewed as well. '), ('9685', 'gastrin_CCK', '', 'gastrin', 'CCK', '6175424', '10', '', '', '', '', '', '', '', '', '', 'VIP-, substance P-, gastrin/CCK-, bombesin-, somatostatin- and glucagon-like immunoreactivities in the gut of the rainbow trout, Salmo gairdneri..     ///    \"Endocrine cells reactive to gastrin/CCK antiserum were demonstrated in the intestinal mucosa, while no immunoreactivity was found in the stomach. \"    ///    \"Radioimmunoassay of stomach mucosa and muscle confirmed the presence of VIP-like and substance P-like immunoreactivity in these tissues, while gastrin/CCK-like immunoreactivity was low and bombesin-like immunoreactivity was insignificant. \"'), ('9686', 'STAT3_JAK2', '', 'STAT3', 'JAK2', '26515594', '10', 'breast cancer\r\r', '', 'Kinase', 'Oncogene', '', 'Receptor', 'Transcription_Factor', '', '', 'Additionally, activation of the JAK2/STAT3 pathway via induction of IL-6 secretion by TrkB enables induction of activation of the EMT program via induction of STAT3 nuclear translocation.     ///    \"Also, TrkB increases Twist-1 and Twist-2 expression through activation of JAK2/STAT3 by inducing c-Src-JAK2 complex formation. \"    ///    \"Furthermore, TrkB in the absence of c-Src binds directly to JAK2 and inhibits SOCS3-mediated JAK2 degradation, resulting in increased total JAK2 and STAT3 levels, which subsequently leads to JAK2/STAT3 activation and Twist-1 upregulation. \"'), ('9687', 'BCR_ABL1', '', 'BCR', 'ABL1', '18408710', '10', '', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'IKZF1 (encoding the transcription factor Ikaros) was deleted in 83.7% of BCR-ABL1 ALL, but not in chronic-phase CML.     ///    \"To define oncogenic lesions that cooperate with BCR-ABL1 to induce ALL, we performed a genome-wide analysis of diagnostic leukaemia samples from 304 individuals with ALL, including 43 BCR-ABL1 B-progenitor ALLs and 23 CML cases. \"    ///    \" The Philadelphia chromosome, a chromosomal abnormality that encodes BCR-ABL1, is the defining lesion of chronic myelogenous leukaemia (CML) and a subset of acute lymphoblastic leukaemia (ALL). \"    ///    These findings suggest that genetic lesions resulting in the loss of Ikaros function are an important event in the development of BCR-ABL1 ALL..     ///    BCR-ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros.. '), ('9688', 'MAPK14_JNK', '', 'MAPK14', 'JNK', '15701637', '10', '', '', 'Kinase', '', '', '', 'Transcription_Factor', '', '', 'Tumor necrosis factor alpha-induced desumoylation and cytoplasmic translocation of homeodomain-interacting protein kinase 1 are critical for apoptosis signal-regulating kinase 1-JNK/p38 activation..     ///    \"A specific JNK inhibitor blocked the reverse but not the initial translocation of HIPK1, suggesting that the initial translocation is an upstream event of ASK1-JNK/p38 signaling and JNK activation regulates the reverse translocation as a feedback mechanism. \"    ///    The kinetics of HIPK1 translocation correlates with those of stress-induced ASK1-JNK/P38 activation.     ///    Our study suggests that TNFalpha-induced desumoylation and cytoplasmic translocation of HIPK1 are critical in TNFalpha-induced ASK1-JNK/p38 activation..     ///    \"Moreover, a sumoylation-defective mutant of HIPK1 (KR5) localizes to the cytoplasm and is constitutively active in ASK1-JNK/P38 activation. \"    ///    \"Consistently, expression of HIPK1 increased, whereas expression of a kinase-inactive form (HIPK1-D315N) or small interference RNA of HIPK1 decreased stress-induced ASK1-JNK/P38 activation without effects on IKK-NF-kappaB signaling. \"    ///     The apoptosis signal-regulating kinase 1 (ASK1)-JNK/p38 signaling pathway is pivotal component in cell apoptosis and can be activated by a variety of death stimuli including tumor necrosis factor (TNF) alpha and oxidative stress (reactive oxygen species). '), ('9689', 'SSX_SS18', '', 'SSX', 'SS18', '23664540', '10', 'soft tissue sarcoma;synovial sarcoma', '', '', '', '', '', '', '', '', 'No associations were found between PFS and gender, body mass index, tumor site, SS18-SSX translocation, or FGFR4 expression. '), ('9690', 'P2Y5_LPA', '', 'P2Y5', 'LPA', '22431770', '10', '', '', '', '', '', '', '', '', '', 'Retraction of: p2y5/LPA? attenuates LPA1-mediated VE-cadherin translocation and cell-cell dissociation through G(12/13) protein-Src-Rap1.. '), ('9691', 'P47_NOX2', '', 'P47', 'NOX2', '24569874', '10', '', '', '', '', '', '', '', '', '', 'The anti-oxidants N-acetyl L-cysteine and Trolox, the p47(phox)-NOX2 NADPH oxidase inhibitory peptide gp91-ds-tat or p47(phox) knockdown each reduced insulin-dependent GLUT4myc translocation. '), ('9692', 'IL23_IL17', '', 'IL23', 'IL17', '26375893', '10', 'periodontal pockets;periodontitis', '', '', '', '', '', '', '', '', 'It is concluded that the bacteria serve as initial triggers for local immunopathology through translocation of bacterial products into the underlying tissues where they unleash the dysregulated IL-23-IL-17 axis.     ///    \"Subsequently, the IL-23/IL-17 inflammatory response sustains and shapes a unique local microbiome which, in turn, can further exacerbate inflammation and bone loss in the susceptible host. \"'), ('9693', 'P65_NFKB1', '', 'P65', 'NFKB1', '10848576', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'Consistent with a role for Src in regulating NF-kappaB activation, an absence of Src activity impaired recruitment of PKC-iota into an IKK complex and markedly impaired NGF-induced translocation of p65/NF-kappaB to the nucleus. '), ('9694', 'PP19_CFL1', '', 'PP19', 'CFL1', '8666784', '10', '', '', '', '', '', '', '', '', '', ' In untransformed T lymphocytes, pp19/cofilin, a cytoplasmic actin-binding protein, undergoes dephosphorylation and nuclear translocation in response to costimulation through accessory receptors (e.g., CD2), but not following TCR/CD3 triggering.     ///    \"In malignant T lymphoma cells, dephosphorylation and nuclear translocation of pp19/cofilin occur spontaneously through constitutive activation of a serine phosphatase. \"    ///    Inhibition of constitutive serine phosphatase activity in T lymphoma cells results in phosphorylation of pp19/cofilin and induces apoptosis..     ///    \"Moreover, lowering the intracellular pp19/cofilin concentrations by antisense-cofilin transfection results in reduced cloning efficiencies. \"    ///    These findings provide support for the view that pp19/cofilin plays a critical role in the growth and survival of both untransformed and malignant T lymphocytes.. '), ('9695', 'MAPK14_JNK', '', 'MAPK14', 'JNK', '22609942', '10', '', '', 'Kinase', '', '', '', 'Transcription_Factor', '', '', 'We show that XJP-1 down-regulates ox-LDL-induced over-expression of adhesion molecules (ICAM-1 and VCAM-1) in a dose-dependent manner in human umbilical vein endothelial cells (HUVECs), attenuates ox-LDL-induced up-regulation of low-density lipoprotein receptor (LOX)-1, decreases generation of reactive oxygen species (ROS), blocks translocation of nuclear factor-kappa B (NF-?B) activity, and prevents activation of c-Jun N-terminal kinase (JNK)/p38 pathways in endothelial cells. ');
INSERT INTO `ChimerPub_dump` VALUES ('9696', 'RET_PTC', '', 'RET', 'PTC', '19415957', '10', 'papillary carcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'It appears that there can be molecular contributions from the RET/PTC translocations and from mutations in the APC gene and beta-catenin gene, which are both part of the Wnt signaling pathway. '), ('9697', 'WAF1_CIP1', '', 'WAF1', 'CIP1', '24935604', '10', '', '', '', '', '', '', '', '', '', '8-60hIPP5(m)-induced G2/M cell cycle arrest involves activation of ATM/p53/p21(cip1/waf1) pathways and delayed cyclin B1 nuclear translocation..     ///    \"Flow cytometric and biochemical analyses showed that overexpression of 8-60hIPP5(m) induced G2/M-phase arrest, which was accompanied by the upregulation of cyclin B1 and phosphorylation of G2/M-phase proteins ATM, p53, p21(cip1/waf1) and Cdc2, suggesting that 8-60hIPP5(m) induces G2/M arrest through activation of the ATM/p53/p21(cip1/waf1)/Cdc2/ cyclin B1 pathways. \"'), ('9698', 'SMAD3_DELTA3', '', 'SMAD3', 'DELTA3', '14980711', '10', 'fibrosarcoma;sarcoma\r\r', 'PCR', '', '', 'Tumor_suppressor', '', 'Transcription_Factor', '', '', 'When smad3-Delta3 is overexpressed in a fibrosarcoma cell line, the Smad3-Delta3 is translocated to the nucleus upon TGF-beta stimulation and binds the Smad responsive element.     ///    \"Using a CAGA luciferase reporter system, we demonstrate that Smad3-Delta3 has transcriptional activity and we conclude that Smad3-Delta3 possesses functional transactivating properties.. \"    ///    Real-time PCR analyses demonstrated that the fraction of smad3-Delta3 mRNA compared to normal smad3 varies between tissues.     ///    We could detect mRNA expression of smad3-Delta3 in all investigated human tissues.     ///    The splicing variant (smad3-Delta3) lacks exon 3 resulting in a truncated linker region. '), ('9699', 'ASK1_JNK', '', 'ASK1', 'JNK', '15701637', '10', '', '', '', '', '', '', '', '', '', 'Tumor necrosis factor alpha-induced desumoylation and cytoplasmic translocation of homeodomain-interacting protein kinase 1 are critical for apoptosis signal-regulating kinase 1-JNK/p38 activation..     ///    \"A specific JNK inhibitor blocked the reverse but not the initial translocation of HIPK1, suggesting that the initial translocation is an upstream event of ASK1-JNK/p38 signaling and JNK activation regulates the reverse translocation as a feedback mechanism. \"    ///    The kinetics of HIPK1 translocation correlates with those of stress-induced ASK1-JNK/P38 activation.     ///    Our study suggests that TNFalpha-induced desumoylation and cytoplasmic translocation of HIPK1 are critical in TNFalpha-induced ASK1-JNK/p38 activation..     ///    \"Consistently, expression of HIPK1 increased, whereas expression of a kinase-inactive form (HIPK1-D315N) or small interference RNA of HIPK1 decreased stress-induced ASK1-JNK/P38 activation without effects on IKK-NF-kappaB signaling. \"    ///     The apoptosis signal-regulating kinase 1 (ASK1)-JNK/p38 signaling pathway is pivotal component in cell apoptosis and can be activated by a variety of death stimuli including tumor necrosis factor (TNF) alpha and oxidative stress (reactive oxygen species).     ///    \"Moreover, a sumoylation-defective mutant of HIPK1 (KR5) localizes to the cytoplasm and is constitutively active in ASK1-JNK/P38 activation. \"'), ('9700', 'CDC7_CRM1', '', 'CDC7', 'CRM1', '17711849', '10', '', '', 'Kinase', '', '', '', '', '', '', 'The primary function of the Cdc7-CRM1 association may be to translocate nuclear Cdc7 to the cytoplasm. '), ('9701', 'SAPK_JNK', '', 'SAPK', 'JNK', '19107874', '10', '', '', '', '', '', '', '', '', '', 'This suggests that aged HDF cells are resistant to oxidative stress by blocking the translocation of Hsp60 from the mitochondria to the cytosol followed by SAPK/JNK inhibition.     ///    \"Overall, the mechanism of resistance by oxidative stress in aged cells is induced by blocked of the translocation of Hsp60 followed by SAPK/JNK inactivation.. \"    ///    The inhibition of SAPK/JNK activation by SP600125 under oxidative stress almost completely blocked the translocation of Hsp60 in both young and aged cells.     ///    The present study showed that the translocation of Hsp60 from the mitochondria to the cytosol followed by high levels of p-SAPK/JNK activation as a result of oxidative stress was observed in the young cells only.     ///    Oxidative stress resistance through blocking Hsp60 translocation followed by SAPK/JNK inhibition in aged human diploid fibroblasts..     ///     The stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) pathway is a well-known senescence-related stress activated protein kinase. '), ('9702', 'JJAZ1_JAZF1', '', 'JJAZ1', 'JAZF1', '25299308', '10', 'endometrial stromal tumor', '', '', '', '', '', '', '', '', 'Specifically, the JAZF1-SUZ12 (formerly JAZF1-JJAZ1) fusion identifies a large proportion of ESN and LG-ESSs, whereas the YWHAE-FAM22 translocation identifies HG-ESSs. '), ('9703', 'KU80_KU70', '', 'KU80', 'KU70', '20023628', '10', '', '', '', '', '', '', '', '', '', 'It phosphorylates a wide range of substrates in vitro, including Ku70/Ku80, which is translocated along DNA.     ///    \"DNA-dependent protein kinase (DNA-PK), a holoenzyme that comprises the DNA-PK catalytic subunit (DNA-PKcs) and the heterodimer Ku70/Ku80, has a major role in non-homologous end joining-the main pathway in mammals used to repair double-strand breaks. \"'), ('9704', 'PPARG_PAX8', '', 'PPARG', 'PAX8', '16149875', '10', 'papillary carcinoma;mucoepidermoid carcinoma\r\r', '', '', '', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'Specific molecular mutations have been described that can be diagnostically useful or explain, in part, their pathogenesis, including the well-known Ret/PTC and PPARgamma-PAX8 translocations, point mutations in the Ret, Ras and BRAF genes, and loss of heterozygosity of multiple different tumor suppressor genes. '), ('9705', 'P65_NFKB1', '', 'P65', 'NFKB1', '19669392', '10', 'osteoarthritis', '', '', '', '', '', 'Transcription_Factor', '', '', 'Nuclear translocation of NFkappaB-p65 was concomitant with an increase in nuclear fluorescence intensity which reached maximum values at 60 min with IL-1beta (p < 0.001).     ///    Nuclear translocation of NFkappaB-p65 was analysed by immunofluoresence microscopy. '), ('9706', 'MAP_ERK', '', 'MAP', 'ERK', '16452220', '10', 'melanoma\r\r', '', '', '', '', '', '', '', '', 'BAY 43-9006 but not the MAP/ERK kinase inhibitors PD98059 or U0126 induced the nuclear translocation of apoptosis-inducing factor (AIF) in A2058 and SKMEL5 cells, and the introduction of a small interfering RNA (siRNA) for AIF partially protected these cells from BAY 43-9006-induced apoptosis. '), ('9707', 'NUP98_HOXD13', '', 'NUP98', 'HOXD13', '26637787', '10', 'myelodysplastic syndrome', '', '', 'Oncogene', '', '', '', 'KB', 'Seq', 'Here, we study the BMME in MDS in vivo using a transgenic murine model of MDS with hematopoietic expression of the translocation product NUP98-HOXD13 (NHD13). '), ('9708', 'MAGI3_AKT3', '', 'MAGI3', 'AKT3', '22722202', '10', 'breast cancer', '', 'Kinase', '', '', '', '', 'KB', '', 'Furthermore, we have identified a recurrent MAGI3-AKT3 fusion enriched in triple-negative breast cancer lacking oestrogen and progesterone receptors and ERBB2 expression.     ///    \"The MAGI3-AKT3 fusion leads to constitutive activation of AKT kinase, which is abolished by treatment with an ATP-competitive AKT small-molecule inhibitor.. \"'), ('9709', 'HDM2_ARF', '', 'HDM2', 'ARF', '16267006', '10', '', '', '', '', '', '', '', '', '', 'We find that DNA damage disrupts the interaction of ARF with the nucleolar protein B23(nucleophosmin) and promotes a transient p53-independent translocation of ARF to the nucleoplasm, resulting in a masking of the ARF NH2 terminus that correlates with the appearance of ARF-Hdm2 complexes.    ///    \"We find that DNA damage disrupts the interaction of ARF with the nucleolar protein B23(nucleophosmin) and promotes a transient p53-independent translocation of ARF to the nucleoplasm, resulting in a masking of the ARF NH2 terminus that correlates with the appearance of ARF-Hdm2 complexes. \"'), ('9710', 'CDKN2B_CDKN2A', '', 'CDKN2B', 'CDKN2A', '21889780', '10', 'astrocytoma;neurofibroma;tuberous sclerosis', '', 'Kinase', '', 'Tumor_suppressor', '', 'Transcription_Factor', '', '', 'TERT, CCDC26, PHLDB1, RTEL1 and CDKN2A/CDKN2B). '), ('9711', 'P65_NFKB1', '', 'P65', 'NFKB1', '18922932', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'We also observed that delphinidin treatment of cells resulted in a dose-dependent decrease in (a) phosphorylation of IkappaB kinase gamma (NEMO), (b) phosphorylation of nuclear factor-kappaB (NF-kappaB) inhibitory protein IkappaBalpha, (c) phosphorylation of NF-kappaB/p65 at Ser(536) and NF-kappaB/p50 at Ser(529), (d) NF-kappaB/p65 nuclear translocation, and (e) NF-kappaB DNA binding activity.     ///    \"Analysis of tumors from delphinidin-treated mice showed significant decrease in the expression of NF-kappaB/p65, Bcl2, Ki67, and PCNA. \"'), ('9712', 'CDH1_APC', '', 'CDH1', 'APC', '21212736', '10', '', '', '', '', 'Tumor_suppressor', '', '', '', '', 'Using a combinatorial approach of immunocytochemistry, biochemical-fraction-coupled immunoprecipitation, mutagenesis as well as protein degradation assay, we have demonstrated that the TGF?-induced Skp2 nucleus translocation is critical for TGF? cytostatic effect that allows physical interaction between Cdh1 and Skp2 and in turn facilitates the Skp2 ubquitylation by Cdh1/APC.     ///    \"Previous observation from immunocytochemistry indicates that Cdh1 principally localizes in the nucleus while Skp2 mainly localizes in the cytosol, which leaves us a puzzle on how Skp2 is recognized and then ubiquitylated by Cdh1/APC in response to TGF? stimulation. \"    ///    Our finding reveals a cellular mechanism that facilitates Skp2 ubiquitylation by Cdh1/APC in response to TGF?..     ///    \" Skp2, a F-box protein that determines the substrate specificity for SCF ubiquitin ligase, has recently been demonstrated to be degraded by Cdh1/APC in response to TGF? signaling. \"'), ('9713', 'SESN2_AMPK', '', 'SESN2', 'AMPK', '25701194', '10', '', '', '', '', '', '', '', '', '', 'After nuclear translocation, PTEN induces autophagy, in association with the activation of the p-JUN-SESN2/AMPK pathway, in response to TPT. '), ('9714', 'MYC_IGL', '', 'MYC', 'IGL', '19535347', '10', 'B cell lymphoma;leukemia', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'Overall survival was not different between the MYC-IGH translocation group (n=14) and the MYC-IGK or MYC-IGL translocation group (n=13). '), ('9715', 'BCR_ABL1', '', 'BCR', 'ABL1', '25748621', '10', 'acute myeloid leukemia;acute lymphoblastic leukemia;chronic myeloid leukemia\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'CBF) or BCR-ABL1 fusion and activation of multiple kinases in chronic myeloid leukemia (CML). '), ('9716', 'MEK_ERK', '', 'MEK', 'ERK', '14672351', '10', 'bone resorption', '', '', '', '', '', '', '', '', 'Assays for NF-kappaB nuclear translocation, NF-kappaB reporter gene activity, protein kinase activity, and Western blotting were used to examine the effects of TPA on RANKL-induced NF-kappaB, c-Jun N-terminal kinase (JNK), and MEK/ERK and p38 signal transduction pathways. '), ('9717', 'PPARG_PAX8', '', 'PPARG', 'PAX8', '18251569', '10', 'oligodendroglioma', '', '', '', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'Molecular assays that are currently in use or on the near horizon, including translocation analyses for RET-PTC and PPARgamma-PAX8, point mutation analysis for BRAF and epidermal growth factor receptor, and genetic loss for 1p and 19q, are discussed.. '), ('9718', 'RET_PTC', '', 'RET', 'PTC', '12665650', '10', 'chronic lymphocytic thyroiditis', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'The finding of the RET-PTC translocations in CLT has been reported by two independent groups of investigators, suggesting that the areas of nuclear atypia in CLT are neoplastic rather than reactive. '), ('9719', 'BCLX_BCL2', '', 'BCLX', 'BCL2', '16009721', '10', '', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'As a result of dissociation, Bad is dephosphorylated and translocates to the mitochondria, where it associates with Bcl-2/Bcl-x(L). '), ('9720', 'MYC_IGH', '', 'MYC', 'IGH', '15315756', '10', '', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'Here we report that AID is essential for the c-myc/IgH chromosome translocations induced by IL6..     ///    \"We have examined c-myc/IgH translocations in IL6 transgenic mice that are mutant for activation induced cytidine deaminase (AID), the enzyme that initiates CSR. \"    ///    AID is required for c-myc/IgH chromosome translocations in vivo.. '), ('9721', 'PPARG_PAX8', '', 'PPARG', 'PAX8', '16627918', '10', 'thyroid carcinoma;papillary carcinoma\r\r', '', '', '', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'These include the translocations RET/PTC and PAX8-PPARgamma and point mutations in the BRAF and RAS genes. '), ('9722', 'HSC70_CX43', '', 'HSC70', 'CX43', '26481195', '10', '', '', '', '', '', '', '', '', '', 'Collectively, our findings suggest that, in Cx43 up-regulation, which is most likely an emergency measure, Cx43-Hsc70 interaction regulates cell cycle G1/S progression through a novel mechanism by which Cx43-Hsc70 interaction prevents the nuclear accumulation of p27 through controlling the nuclear translocation of cyclin D1-CDK4-p27 complex. '), ('9723', 'STAT3_EGFR', '', 'STAT3', 'EGFR', '22986230', '10', 'lung cancer\r\r', '', 'Kinase', 'Oncogene', '', 'Receptor', 'Transcription_Factor', '', '', 'In addition, we found that PDT stimulates nuclear translocation of STAT3 and STAT3/EGFR association and that inhibiting STAT3 signaling prior to PDT leads to increased PDT cytotoxicity. '), ('9724', 'TNFA_LPS', '', 'TNFA', 'LPS', '19520742', '10', '', '', '', '', '', '', '', '', '', 'Curcumin inhibited Akt/MAPK/NF-kappaB activity and prevented nuclear translocation of the p65 NF-kappaB subunit following TNF-alpha/LPS.     ///    \"At physiological shear stress, curcumin attenuated leukocyte adhesion to TNF-alpha/LPS-activated HIMEC monolayers. \"'), ('9725', 'JUN_ATF2', '', 'JUN', 'ATF2', '24707477', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'Moreover, CBHA significantly enhanced mitogen-activated protein kinase phosphatase-(MKP-) 5/MKP-1 expression and inhibited p38/JNK activations, ATF2/c-Jun translocation, and PAI-1 promoter activity. '), ('9726', 'RET_PTC', '', 'RET', 'PTC', '16867191', '10', '', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'Molecular studies have found RET/PTC translocations in some examples, supporting HTN as a PTC. '), ('9727', 'PECAM1_PARP1', '', 'PECAM1', 'PARP1', '25793984', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'Low shear stress induced HMGB1 translocation and release via PECAM-1/PARP-1 pathway to induce inflammation response.. '), ('9728', 'MYC_IGH', '', 'MYC', 'IGH', '19535347', '10', 'B cell lymphoma;leukemia', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'Overall survival was not different between the MYC-IGH translocation group (n=14) and the MYC-IGK or MYC-IGL translocation group (n=13).     ///    \"The MIB-1 index was investigated in 14 cases with aggressive B-cell lymphoma, and was higher in the group with MYC-IGH translocation (n=7) than in the MYC-IGK/L group (n=7) (p=0.02). \"'), ('9729', 'SAPK_JNK', '', 'SAPK', 'JNK', '12697421', '10', '', '', '', '', '', '', '', '', '', 'Stimulation of hRPE cells by monocytes resulted in prominent increases in p38, ERK1/2 and JNK/SAPK phosphorolation, IkappaBalpha degradation, and NF-kappaB nuclear translocation.     ///    \"This study investigates chemokine secretion induced by co-culture of hRPE cells and monocytes and illustrates the roles of p38 kinase, ERK, JNK/SAPK and NF-kappaB-inducing kinase signaling pathways for hRPE IL-8 and MCP-1 secretion induced in hRPE by co-culture with monocytes. \"'), ('9730', 'MYC_IGL', '', 'MYC', 'IGL', '21491965', '10', 'B cell lymphoma;lymphoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'In this article, we report a case of an adolescent patient who presented with high-grade breast lymphoma with concurrent BCL2-IGH and MYC-IGL translocations, and we review the clinical, pathological, and genetic features.     ///    Primary high-grade B-cell lymphoma of the breast with concurrent IGH-BCL2 and MYC-IGL translocations in an adolescent patient.. '), ('9731', 'NLRR3_ICD', '', 'NLRR3', 'ICD', '25256744', '10', 'neuroblastoma\r\r', '', '', '', '', '', '', '', '', 'In this study, we have found for the first time that NLRR3 is proteolytically processed by secretases and its intracellular domain (NLRR3-ICD) is then released to translocate into cell nucleus during ATRA-mediated neuroblastoma differentiation.     ///    \"Since the proteolytic cleavage of NLRR3 was blocked by ?- or ?-secretase inhibitor, it is likely that NLRR3-ICD is produced through the secretase-mediated processing of NLRR3. \"    ///    \"According to our present observations, NLRR3-ICD was induced to accumulate in cell nucleus of neuroblastoma SH-SY5Y cells following ATRA treatment. \"    ///    \"Furthermore, overexpression of NLRR3-ICD stimulated ATRA-dependent neurite elongation in SK-N-BE cells. \"    ///    Intracellular fragment of NLRR3 (NLRR3-ICD) stimulates ATRA-dependent neuroblastoma differentiation..     ///    \"Together, our present results strongly suggest that NLRR3-ICD produced by the secretase-mediated proteolytic processing of NLRR3 plays a crucial role in ATRA-mediated neuronal differentiation, and provide a clue to develop a novel therapeutic strategy against aggressive neuroblastomas. \"    ///    \"Intriguingly, forced expression of NLRR3-ICD in neuroblastoma SK-N-BE cells significantly suppressed their proliferation as examined by a live-cell imaging system and colony formation assay. \"'), ('9732', 'PDGFB_COL1A1', '', 'PDGFB', 'COL1A1', '22285046', '10', 'dermatofibrosarcoma protuberans;sarcoma\r\r', '', '', 'Oncogene', '', '', '', 'KB', '', 'COL1A1-PDGFB translocation is specific to dermatofibrosarcoma protuberans, and the presence of this fusion contributes to diagnosis in certain cases. '), ('9733', 'TIMP3_ITGA7', '', 'TIMP3', 'ITGA7', '23830872', '10', 'prostate cancer\r\r', '', '', '', '', '', '', '', '', 'The ITGA7-TIMP3 binding led to a decreased protein level of tumor necrosis factor ?, cytoplasmic translocation of NF-?B, and down-regulation of cyclin D1.     ///    \"Interestingly, knocking down ITGA7 ligand laminin ?1 enhanced ITGA7-TIMP3 signaling and the downstream tumor-suppressor activity, suggesting the existence of a counterbalancing role between extracellular matrix and integrin signaling. \"    ///    \"Knocking down TIMP3 or ITGA7/TIMP3 binding interference largely abrogated the signaling changes induced by ITGA7, whereas a mutant ITGA7 lacking TIMP3 binding activity had no tumor-suppressor activity. \"'), ('9734', 'ENDOG_AIF', '', 'ENDOG', 'AIF', '25048111', '10', '', '', '', '', '', '', '', '', '', 'Our data clearly show that PPAR? activation prevents DNA damage and neuronal cell apoptosis by decreasing the expression and translocation of AIF/Endo G to the nucleus in a caspase-3- and p53-independent pathway in the NT2N cell model. '), ('9735', 'NUP98_HOXA9', '', 'NUP98', 'HOXA9', '17601986', '10', 'myeloid leukemia;leukemia\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', 'Seq', 'Primitive normal hematopoietic cells were modified to express the BCR/ABL and Nup98/HoxA9 translocation products, and a distinct LSC population, with the aberrant immunophenotype of lineage(-), Kit(+/-), Flt3(+), Sca(+), CD34(+), and CD150(-), was identified. '), ('9736', 'NFIB_MYB', '', 'NFIB', 'MYB', '24732452', '10', 'adenoid cystic carcinoma;adenocarcinoma\r\r', '', '', '', '', '', '', 'KB', '', 'Our data further demonstrated that the MYB/NFIB translocation is not necessarily an early event or fundamental for the progression to adenoid cystic carcinoma with high-grade transformation. '), ('9737', 'NUT_NSD3', '', 'NUT', 'NSD3', '26490121', '10', '', '', '', '', '', '', '', '', '', 'Pathological assessment of the biopsy specimens revealed a NUT carcinoma with typical morphological characteristics and an uncommon NUT translocation variant with a NSD3-NUT fusion. '), ('9738', 'TBLR1_TBL1', '', 'TBLR1', 'TBL1', '26369384', '10', 'bladder cancer', '', '', '', '', '', '', '', '', 'WNT ligands induced TBL1/TBLR1 SUMOylation to form complexes with ?-catenin to facilitate ?-catenin nuclear translocation, which could be efficiently inhibited through suppression of SUMOylation of TBL1/TBLR1.     ///    \"Together, our data suggest that SENP2 inhibits MMP13 expression in BC cells through de-SUMOylation of TBL1/TBLR1, which inhibits nuclear translocation of ?-catenin. \"    ///    SENP2 regulates MMP13 expression in a bladder cancer cell line through SUMOylation of TBL1/TBLR1.. '), ('9739', 'HMGB1_BECN1', '', 'HMGB1', 'BECN1', '25607248', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'Moreover, pharmacological inhibition of PARP1 activity or knockdown of PARP1 gene expression significantly inhibited TNFSF10-induced HMGB1 cytoplasmic translocation and subsequent HMGB1-BECN1 complex formation. '), ('9740', 'P53_FOXO3A', '', 'P53', 'FOXO3A', '24954032', '10', '', '', '', '', '', '', '', '', '', 'Thr32 phosphorylation of FoxO3a may promote a translocation of FoxO3a-p53 complex from nucleus to the cytoplasm, and the role of FoxO3a dephosphorylation was further studied. '), ('9741', 'EML4_ALK', '', 'EML4', 'ALK', '24616318', '10', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Optic neuropathy and blindness associated with crizotinib for non-small-cell lung cancer with EML4-ALK translocation.. '), ('9742', 'P65_P50', '', 'P65', 'P50', '21286379', '10', '', '', '', '', '', '', '', '', '', 'As a mechanism of action, PUE increased phosphorylation of ERK, JNK, and p38 MAPKs, and enhanced nuclear translocation of NF-?B p50/p65 in DCs. '), ('9743', 'PAX3_FKHR', 't(2;13)(q35;14) / ', 'PAX3', 'FKHR', '15639120', '10', 'infantile spinal muscular atrophy', '', '', '', '', '', '', '', '', 'Since cell proliferation is increased in de- and regenerating muscle and the PAX3/FKHR fusion protein activates myogenic transcription, it is tempting to speculate whether severe muscle atrophy in SMA might predispose to malignant transformation in long-standing disease.. '), ('9744', 'MLT1_API2', '', 'MLT1', 'API2', '12393483', '10', 'follicular lymphoma;B cell lymphoma;lymphoma\r\r', '', '', '', '', '', '', '', '', 'Most types of low-growth fraction lymphomas are initiated by molecular events resulting in the inhibition of apoptosis, such as translocations affecting BCL2, in follicular lymphoma, or BCL10 and API2/MLT1, in mucosa-associated lymphoid tissue (MALT) lymphomas. '), ('9745', 'P65_P50', '', 'P65', 'P50', '9480845', '10', '', '', '', '', '', '', '', '', '', 'Overexpression of TAK1 together with its activator protein, TAK1 binding protein 1 (TAB1), induced the nuclear translocation of NF-kappa B p50/p65 heterodimer accompanied by the degradation of I kappa B alpha and I kappa B beta, and the expression of kappa B-dependent reporter gene. '), ('9746', 'NUP98_NSD1', '', 'NUP98', 'NSD1', '22929522', '10', '', '', '', '', '', '', 'Transcription_Factor', 'KB', 'Seq', 'Analysis of NUP98/NSD1 translocations in adult AML and MDS patients.. '), ('9747', 'IL1RA_IL1B', '', 'IL1RA', 'IL1B', '7586694', '10', '', 'PCR', '', '', '', '', '', '', '', 'These results suggest that the IL-1 beta/IL-1Ra allelic cluster may participate in defining the biological basis of predisposition to chronic inflammatory bowel diseases.. '), ('9748', 'P65_P50', '', 'P65', 'P50', '23869238', '10', '', '', '', '', '', '', '', '', '', 'BBR also suppressed the nuclear translocation of p50/p65 NF-?B proteins and their binding to COX-2 promoter, causing inhibition of COX-2. '), ('9749', 'ABL1_FE65', '', 'ABL1', 'FE65', '17590240', '10', '', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'Furthermore, EGCG also decreased nuclear translocation of c-Abl and blocked APP-C99-dependent GSK3 beta activation, and these inhibitory effects occurred through the interruption of c-Abl/Fe65 interaction.     ///    Epigallocatechin gallate (EGCG) suppresses beta-amyloid-induced neurotoxicity through inhibiting c-Abl/FE65 nuclear translocation and GSK3 beta activation.. '), ('9750', 'MAPK3_P42', '', 'MAPK3', 'P42', '24441870', '10', '', '', 'Kinase', '', '', '', '', '', '', 'On the other hand, TNF-? could induce Akt and p42/p44 MAPK translocation from the cytosol into the nucleus, which was inhibited by AG490, AG1296, or LY294002.     ///    \"We showed that TNF-? markedly stimulated Jak2, PDGFR, Akt, and p42/p44 MAPK phosphorylation, which were attenuated by their respective inhibitors. \"    ///    \"In addition, TNF-?-induced p42/p44 MAPK phosphorylation was reduced by AG1296 or LY294002. \"'), ('9751', 'MALT1_BIRC3', '', 'MALT1', 'BIRC3', '22890838', '10', 'small cell lymphoma', '', '', '', '', '', '', '', '', 'To further investigate this, we comparatively analyzed samples of two morphologically different regions of the same small cell tumor with a BIRC3-MALT1 translocation, as well as material acquired at two different time points from one composite lymphoma. '), ('9752', 'JUN_AP1', '', 'JUN', 'AP1', '12692090', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'Only at high concentrations, cPG enhanced TNF-alpha-induced cell death and inhibited TNF-alpha-induced IkappaB-alpha kinase (IKK) activation, IkappaB-alpha degradation, and NF-kappaB/p65 translocation, while promoting AP-1/c-jun phosphorylation. '), ('9753', 'MYC_IGH', '', 'MYC', 'IGH', '19966290', '10', 'B cell lymphoma', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'The best characterized of these is c-myc/IgH translocation, which is associated with Burkitt\'s lymphoma.     ///    \"We find that PUMA, Bim, and PKCdelta are required for protection against c-myc/IgH translocation, whereas Bcl-XL and BAFF enhance c-myc/IgH translocation. \"    ///    \"To further define the mechanism of protection against the accumulation of cells that bear c-myc/IgH translocation, we assayed B cells from mice that carry mutations in cell-cycle and apoptosis regulator proteins that act downstream of p53. \"    ///    Whether these effects are general or specific to c-myc/IgH translocation and whether AID produces dsDNA breaks in genes other than c-myc and Ig is not known.     ///    \"Igbeta/IgH, like c-myc/IgH translocations, are AID-dependent, and AID is responsible for lesions on IgH and the non-IgH translocation partners. \"    ///    \"c-myc/IgH translocations are rare events, in part because ATM, p53, and p19 actively suppress them. \"'), ('9754', 'NEU_ERBB2', '', 'NEU', 'ERBB2', '16865267', '10', '', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'The baseline nuclear translocation of AP-1 and pCREB was particularly evident in M13SV1R2N1 cells and was further enhanced by DMBA treatment, indicating an interaction between c-erbB2/neu and DMBA-induced signalling.     ///    \"Further cell lines were derived following sequential transfection with SV40 large T-antigen (immortal, non-tumorigenic M13SV1 cells), exposure to X-rays (weakly tumorigenic M13SV1R2 cells), and ectopic expression of c-erbB2/neu (highly tumorigenic M13SV1R2N1 cells). \"'), ('9755', 'P65_NFKB1', '', 'P65', 'NFKB1', '12970933', '10', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'This effect on NF-kappaB/p65 nuclear translocation was in a concentration dependent manner.     ///    The expression of NF-kappaB/p65 in nuclei was measured by Western-blot analysis.     ///    The FITC-label NF-kappaB/p65 was mainly located in the nuclei after THP-1 cells were stimulated with LPS. '), ('9756', 'P53_H2AX', '', 'P53', 'H2AX', '14712078', '10', 'ataxia telangiectasia;Bloom syndrome;Nijmegen breakage syndrome', '', '', '', '', '', '', '', '', 'Here, we summarize H2AX functions and outline a specific \"anchoring\" model, that can explain the translocation prone phenotype of H2AX-deficient and H2AX/p53-deficient mice. '), ('9757', 'P67_P47', '', 'P67', 'P47', '19222497', '10', '', '', '', '', '', '', '', '', '', 'TauCl but not taurine inhibited p47phox-p67phox translocation.     ///    \"The effects of TauCl and taurine (0.1-1 mM) were investigated on the generation of superoxide anion (ferricytochrome-c reduction microassay), calcium signal (fluorimetry), p47phox-p67phox translocation (Western blot), leukotriene C4 (LTC4) production (enzymeimmunoassay), eosinophil peroxidase (EPO) release (spectrophotometry), eosinophil cationic protein (ECP) release (radioimmunoassay), apoptosis (flow cytometry with annexin V-propidium iodide), and nuclear factor-kappaB (NF-kappaB) activation (Western blot). \"'), ('9758', 'TNFA_TNFR1', '', 'TNFA', 'TNFR1', '18710428', '10', 'cholangiocarcinoma', '', '', '', '', '', '', '', '', 'These data suggest that TNF-alpha/TNF-R1 interaction leads to the phosphorylation of Erk1/2 and p38MAPK and nuclear translocation of NF-kappaB, which is closely associated with the production and activation of MMP-9 in cultured CC cells of HuCTT-1 and CCKS-1. '), ('9759', 'STAT6_NAB2', '', 'STAT6', 'NAB2', '23661264', '10', 'synovial sarcoma;liposarcoma;rhabdomyosarcoma;solitary fibrous tumor;sarcoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', '', 'Recently identified novel druggable targets include the MDM2 amplifications in well-differentiated and dedifferentiated liposarcomas, the new translocation NAB2:STAT6 of solitary fibrous tumors, the angiopoeitin-TIE2 pathway in angiosarcoma, the suppression of Mcl1 in X:18/synovial sarcomas, the mTOR pathway in malignant peripheral nerve sheath tumors, CDK4 in alveolar rhabdomyosarcoma, cMET regulation in alveolar soft parts sarcoma, the metabolic abnormalities in wild-type/SHD GIST, and the lack of argininosuccinate synthetase 1 expression seen in most sarcomas. '), ('9760', 'NAPA_DP', '', 'NAPA', 'DP', '3546306', '10', '', '', '', '', '', '', '', '', '', ' The translocation of occupied surface insulin receptors to the nuclei of isolated hepatocytes was studied using the biologically active photosensitive insulin derivative, B2(2-nitro-4-azidophenylacetyl)-des-PheB1-insulin (NAPA-DP-insulin). '), ('9761', 'MDR1_P-gp', '', 'MDR1', 'P-gp', '21300134', '10', 'B cell lymphoma;lymphoma\r\r', '', '', '', '', '', '', '', '', 'Doxorubicin can increase expression of mdr1/P-glycoprotein through activating MAPK/ERK transduction pathway, then increasing expression of YB-1, inducing YB-1 nuclear translocation, and enhancing DNA-binding activity of YB-1.. '), ('9762', 'DRD2_ANKK1', '', 'DRD2', 'ANKK1', '25684044', '10', 'alcohol dependence', 'PCR', 'Kinase', '', '', 'Receptor', '', '', '', 'However, for the DRD2/ANKK1 SNP does not present contributions to the development of AD..     ///    \"However, there was no statistically significant difference when the allelic (p?=?0.10) and genotypic (p?>?0.05) frequencies for DRD2/ANKK1 Taq1A were compared. \"    ///    \"Genotyping was detected through polymerase chain reaction (PCR) for SLC6A3 40?bp-VNTR and RFLP-PCR for DRD2/ANKK1 Taq1A, and subsequent electrophoresis on a 2% agarose gel. \"    ///    Association study of the SLC6A3 VNTR (DAT) and DRD2/ANKK1 Taq1A polymorphisms with alcohol dependence in a population from northeastern Brazil..     ///    \"The aim of this search was to test the association of the SLC6A3 40?bp-VNTR and DRD2/ANKK1 Taq1A single nucleotide polymorphism (SNP), a transporter and receptor of the dopaminergic system, with AD through a study in a population of northeastern Brazil. \"'), ('9763', 'RET_PTC', '', 'RET', 'PTC', '16627918', '10', 'thyroid carcinoma;papillary carcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'These include the translocations RET/PTC and PAX8-PPARgamma and point mutations in the BRAF and RAS genes. '), ('9764', 'TNF_IL6', '', 'TNF', 'IL6', '22301607', '10', '', '', '', '', '', '', '', '', '', 'Inhibition of GEF-H1 by specific small interfering RNA or inactivation of Rho-associated kinase with Y-27632 not only significantly reduced LPS-induced p38 and extracellular signal-regulated kinase 1/2 (ERK1/2) activities but also blocked LPS-induced NF-?B translocation and activation, thereby inhibiting IL-6/TNF-? mRNA and protein productions.     ///    \"Specific inactivation of RhoA/Cdc42/Rac1 by Clostridium difficile toxin B-10463 (TcdB-10463) reduced LPS-induced nuclear factor ?B (NF-?B) p65 phosphorylation, IL-6/TNF-? messenger RNA (mRNA), and IL-6/TNF-? protein productions. \"    ///    \"Activated Rho-associated kinase by GEF-H1 subsequently activates p38 and ERK1/2, thereby increasing IL-6/TNF-? expression in endothelial cells. \"    ///    \"however, both inhibitors significantly suppressed IL-6/TNF-? mRNA and protein expression. \"    ///    \"P38 and ERK1/2 regulate LPS-induced IL-6/TNF-? expression through an NF-?B-dependent manner and an NF-?B-independent manner, respectively.. \"    ///    \"Using human umbilical vein endothelial cells, we analyzed the role of guanine-nucleotide exchange factor H1 (GEF-H1) on lipopolysaccharide (LPS)-dependent IL-6/TNF-? expression in endothelial cells. \"'), ('9765', 'MAPK3_P42', '', 'MAPK3', 'P42', '9700154', '10', '', '', 'Kinase', '', '', '', '', '', '', 'We have previously shown that the activation of p42/p44 MAPK required for transduction of mitogenic signaling is associated with a rapid nuclear translocation of these kinases.     ///    We therefore conclude that the MAPK nuclear translocation requires both activation of the p42/p44 MAPK module and neosynthesis of short-lived proteins that we postulate to be nuclear anchors..     ///    \"In this study, we have demonstrated that activation of the p42/ p44 MAPK pathway was necessary and sufficient for triggering nuclear translocation of p42 and p44 MAPK. \"    ///    Growth factor-induced p42/p44 MAPK nuclear translocation and retention requires both MAPK activation and neosynthesis of nuclear anchoring proteins..     ///    \" Mitogen-activated protein kinases (p42/p44 MAPK, also called Erk2 and Erk1) are key mediators of signal transduction from the cell surface to the nucleus. \"    ///    \"Indeed, inhibitors of protein synthesis abrogate nuclear accumulation in response to serum and accelerate p42/p44 MAPK nuclear efflux under conditions of persistent p42/p44 MAPK activation. \"    ///    \"In contrast, inhibition of targeted proteolysis by the proteasome synergistically potentiated p42/p44 MAPK nuclear localization by nonmitogenic agonists and markedly prolonged nuclear localization of p42/p44 MAPK after mitogenic stimulation. \"    ///    \"In addition, we have shown that this nuclear accumulation of p42/p44 MAPK required the neosynthesis of short-lived proteins. \"    ///    \"First, addition of the MEK inhibitor PD 98059, which blocks activation of the p42/p44 MAPK pathway, impedes the nuclear accumulation, whereas direct activation of the p42/p44 MAPK pathway by the chimera DeltaRaf-1:ER is sufficient to promote nuclear accumulation of p42/p44 MAPK. \"'), ('9766', 'P65_P50', '', 'P65', 'P50', '14602581', '10', '', '', '', '', '', '', '', '', '', 'Pretreatment with EGF protected monolayers by increasing native PKC-beta1 activity, decreasing IkappaBalpha phosphorylation/degradation, suppressing NF-kappaB activation (p50/p65 subunit nuclear translocation/activity), enhancing stable actin (increased F-actin-to-G-actin ratio), increasing stability of actin cytoskeleton, and reducing barrier hyperpermeability. '), ('9767', 'CCNB1_CDK1', '', 'CCNB1', 'CDK1', '22726437', '10', '', '', 'Kinase', '', '', '', '', '', '', ' Mitosis is triggered by the activation of Cdk1-cyclin B1 and its translocation from the cytoplasm to the nucleus.     ///    \"Interfering with the abruptness of Cdk1-cyclin B1 translocation affects the timing and synchronicity of subsequent mitotic events, underscoring the functional importance of this feedback. \"    ///    We used chemical biology approaches and live-cell microscopy to show that nuclear Cdk1-cyclin B1 promotes the translocation of Cdk1-cyclin B1 to the nucleus.     ///    Positive feedback loops regulate the activation of Cdk1-cyclin B1 and help make the process irreversible and all-or-none in character.     ///    \"Here we examine whether an analogous process, spatial positive feedback, regulates Cdk1-cyclin B1 redistribution. \"'), ('9768', 'TLR4_MYD88', '', 'TLR4', 'MYD88', '24050190', '10', '', '', '', 'Oncogene', '', '', '', '', '', 'In addition, LPS activated nuclear factor-?B (NF-?B) via a TLR4/MyD88-dependent manner and inhibited BMP-2-induced phosphorylation and nuclear translocation of Smad1/5/8. '), ('9769', 'PBX1_E2A', 't(1;19)  / ', 'PBX1', 'E2A', '9310317', '10', 'precursor B cell leukemia', '', '', '', '', '', 'Transcription_Factor', '', '', 'The E2A-Pbx1 fusion protein should therefore activate transcription of genes normally regulated by Pbx1. '), ('9770', 'EML4_ALK', '', 'EML4', 'ALK', '23728235', '10', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'For example, patients with activating EGFR mutations or EML4-ALK translocations largely benefit from targeted therapies with tyrosine kinase inhibitors with better response rates and progression-free survival compared to standard chemotherapy regimens. '), ('9771', 'EWSR1_CHN', '', 'EWSR1', 'CHN', '23058004', '10', 'chondrosarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'In both cases diagnosis was confirmed by the presence of the typical EWSR1-CHN translocation.     ///    \"  Extraskeletal myxoid chondrosarcoma (EMCS) is a rare soft tissue sarcoma of uncertain differentiation, characterized in most cases by a translocation that results in the fusion protein EWSR1-CHN (the latter even called NR4A3 or TEC). \"'), ('9772', 'SMAD4_SMAD1', '', 'SMAD4', 'SMAD1', '20701465', '10', '', '', '', '', 'Tumor_suppressor', '', 'Transcription_Factor', '', '', 'In addition, no BMP-induced nuclear translocation of Smad1/Smad4 complexes could be discerned, suggesting that the canonical BMP2 signaling pathway may not be functional in ASCs. '), ('9773', 'TMPRSS2_ERG', '', 'TMPRSS2', 'ERG', '23872663', '10', 'prostate cancer\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'Recent studies, however, suggest that genetic differences, such as the lower incidence of Chinese prostate cancers harboring TMPRSS2-ERG translocations compared to patients from Western countries, should be carefully considered in the context of genotypic and phenotypic differences among interracial groups. '), ('9774', 'MEK1_ERK', '', 'MEK1', 'ERK', '16634370', '10', 'antiphospholipid syndrome\r\r', '', '', '', '', '', '', '', '', 'In a recent study, we have demonstrated that aPL induces TF expression in monocytes from APS patients by activating, simultaneously and independently, the phosphorylation of MEK-1/ERK proteins, and the p38 MAP kinase-depenent nuclear translocation and activation of NFkappaB/Rel proteins. '), ('9775', 'TEL_AML1', '', 'TEL', 'AML1', '15142881', '10', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'Among 113 children with newly diagnosed ALL, lymphoblasts with the TEL-AML1 translocation had significantly lower DNPS than all other genetic subtypes of B-lineage ALL or T-lineage ALL (352 +/- 57 versus 1001 +/- 31 or versus 1315 +/- 76 fmol/nmol/h, P <.0001).     ///    These findings have established that TEL-AML1 ALL has significantly lower de novo purine synthesis and differential expression of genes involved in purine metabolism..     ///    \"Differentially expressed genes included HPRT, IMPDH, PAICS, and GART, all of which were expressed at a significantly lower level in TEL-AML1 ALL. \"    ///    Acute lymphoblastic leukemia with TEL-AML1 fusion has lower expression of genes involved in purine metabolism and lower de novo purine synthesis.. '), ('9776', 'SAPK_JNK', '', 'SAPK', 'JNK', '11467837', '10', '', '', '', '', '', '', '', '', '', 'The data demonstrate that smooth muscle cells are targets for angiogenin and that both SAPK/JNK phosphorylation and nuclear translocation of the ligand are required for angiogenin to activate smooth muscle cells..     ///    Neomycin inhibits nuclear translocation of angiogenin and abolishes angiogenin-induced cell proliferation but does not inhibit SAPK/JNK phosphorylation.     ///    This activity of angiogenin depends on the cell density and requires nuclear translocation of the ligand as well as activation of SAPK/JNK MAP kinase.     ///    Angiogenin binds to a 170-kDa putative receptor on the cell surface and induces phosphorylation of SAPK/JNK. '), ('9777', 'SIAH1_GAPDH', '', 'SIAH1', 'GAPDH', '15951807', '10', '', '', '', '', '', '', '', '', '', 'Activation of macrophages by endotoxin and of neurons by glutamate elicits GAPDH-Siah1 binding, nuclear translocation and apoptosis, which are prevented by NO deletion. '), ('9778', 'EML4_ALK', '', 'EML4', 'ALK', '26076869', '10', 'small cell carcinoma;lung cancer;adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The main oncogenic factors in the field of thoracic oncology are mutations of EGFR, KRAS, and EML4-ALK translocation, which are most often reported in adenocarcinomas. '), ('9779', 'MET_HGF', '', 'MET', 'HGF', '24959084', '10', '', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'The HGF-MET axis is frequently dysregulated in cancer by MET gene amplification, translocation, and mutation, or by MET or HGF protein overexpression.     ///    \"This review summarizes the key biological features of the HGF-MET axis, its dysregulation in cancer, and the therapeutic agents targeting the HGF-MET axis, which are in development. \"    ///    The potential roles of hepatocyte growth factor (HGF)-MET pathway inhibitors in cancer treatment..     ///    Targeting the dysregulated HGF-MET pathway is an area of active research. '), ('9780', 'TCF3_PBX1', '', 'TCF3', 'PBX1', '24135088', '9', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia;hematopoietic malignancy\r\r', '', '', '', '', '', 'Transcription_Factor', 'KB', 'Seq', 'Based on this observation, we propose this sequence is important for the oncogenesis of TCF3-PBX1 acute lymphoblastic leukemia..    ///    Translocation junctions in TCF3-PBX1 acute lymphoblastic leukemia/lymphoma cluster near transposable elements..     ///    \"Based on this observation, we propose this sequence is important for the oncogenesis of TCF3-PBX1 acute lymphoblastic leukemia.. \"'), ('9781', 'PAX7_FOXO1A', '', 'PAX7', 'FOXO1A', '22710712', '9', 'rhabdomyosarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Chromatin immunoprecipitation on the myogenin promoter showed that PAX3/FOXO1A or PAX7/FOXO1A did not prevent MyoD from binding.    ///    These translocations create chimeric transcription factors termed PAX3/FOXO1A and PAX7/FOXO1A respectively.'), ('9782', 'CLTC_ALK', 't(2;17)(p23;q23) / ', 'CLTC', 'ALK', '15492998', '9', 'B cell lymphoma;lymphoma\r\r', 'PCR;RT-PCR', 'Kinase', 'Oncogene', '', '', '', 'KB', '', 'This report describes a primary gastric ALK-positive B-lineage lymphoma in which a clathrin (CLTC)-ALK fusion was identified by RT-PCR and direct sequencing of the breakpoint. '), ('9783', 'TPM3_ALK', '', 'TPM3', 'ALK', '18660380', '8', 'juvenile xanthogranuloma', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'One case successfully analyzed by molecular techniques revealed TPM3-ALK fusion.    ///    One case successfully analyzed by molecular techniques revealed TPM3-ALK fusion. '), ('9784', 'SYT_SSX2', '', 'SYT', 'SSX2', '17334332', '8', 'synovial sarcoma;rhabdomyosarcoma;ewing sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Real-time RT-PCR assays specific for Ewing\'s sarcoma (EWS-FLI1, EWS-ERG, EWS-ETV1, EWS-ETV4, and EWS-FEV), synovial sarcoma (SYT-SSX1 and SYT-SSX2), and rhabdomyosarcoma (PAX3-FKHR and PAX7-FKHR) were tested across the samples. '), ('9785', 'FUS_CHOP', 't(12;16)(q13;p11) / ', 'FUS', 'CHOP', '7987849', '8', 'liposarcoma;sarcoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'In the present study, we have mapped 16 genomic breakpoints in the region of the CHOP gene and isolated and sequenced a new variant (type II) of the chimeric FUS/CHOP transcript. '), ('9786', 'EWS_ETV4', '', 'EWS', 'ETV4', '17334332', '8', 'synovial sarcoma;rhabdomyosarcoma;ewing sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Real-time RT-PCR assays specific for Ewing\'s sarcoma (EWS-FLI1, EWS-ERG, EWS-ETV1, EWS-ETV4, and EWS-FEV), synovial sarcoma (SYT-SSX1 and SYT-SSX2), and rhabdomyosarcoma (PAX3-FKHR and PAX7-FKHR) were tested across the samples. '), ('9787', 'PAX3_FKHR', '', 'PAX3', 'FKHR', '17334332', '8', 'synovial sarcoma;rhabdomyosarcoma;ewing sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Real-time RT-PCR assays specific for Ewing\'s sarcoma (EWS-FLI1, EWS-ERG, EWS-ETV1, EWS-ETV4, and EWS-FEV), synovial sarcoma (SYT-SSX1 and SYT-SSX2), and rhabdomyosarcoma (PAX3-FKHR and PAX7-FKHR) were tested across the samples. '), ('9788', 'PAX7_FKHR', '', 'PAX7', 'FKHR', '17334332', '8', 'synovial sarcoma;rhabdomyosarcoma;ewing sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Real-time RT-PCR assays specific for Ewing\'s sarcoma (EWS-FLI1, EWS-ERG, EWS-ETV1, EWS-ETV4, and EWS-FEV), synovial sarcoma (SYT-SSX1 and SYT-SSX2), and rhabdomyosarcoma (PAX3-FKHR and PAX7-FKHR) were tested across the samples. '), ('9789', 'ETV6_AML1', 't(12;21)(p13;q22) / t(12;21)  / t(12;21) / ', 'ETV6', 'AML1', '10914546', '8', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'ETV6/AML1 ALLs identification.. '), ('9790', 'WT1_EWS', 't(11;22)(p13;q12) / ', 'WT1', 'EWS', '9949226', '8', 'desmoplastic small round cell tumor \r\r', '', '', '', '', '', '', '', '', 'We report here the first case of DSRCT with a variant EWS-WT1 chimeric product that includes 9 exons of EWS and 3 exons of WT1.. '), ('9791', 'FEV_EWS', '', 'FEV', 'EWS', '17334332', '8', 'synovial sarcoma;rhabdomyosarcoma;ewing sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Real-time RT-PCR assays specific for Ewing\'s sarcoma (EWS-FLI1, EWS-ERG, EWS-ETV1, EWS-ETV4, and EWS-FEV), synovial sarcoma (SYT-SSX1 and SYT-SSX2), and rhabdomyosarcoma (PAX3-FKHR and PAX7-FKHR) were tested across the samples. '), ('9792', 'SYT_SSX1', '', 'SYT', 'SSX1', '17334332', '8', 'synovial sarcoma;rhabdomyosarcoma;ewing sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Real-time RT-PCR assays specific for Ewing\'s sarcoma (EWS-FLI1, EWS-ERG, EWS-ETV1, EWS-ETV4, and EWS-FEV), synovial sarcoma (SYT-SSX1 and SYT-SSX2), and rhabdomyosarcoma (PAX3-FKHR and PAX7-FKHR) were tested across the samples. '), ('9793', 'RLF_MYCL', '', 'RLF', 'MYCL', '8545128', '7', '', '', '', '', '', '', '', '', '', 'The zinc fingers are not contained in the 79 amino acid N-terminal region of RLF involved in the RLF-L-myc fusions, and the transforming ability of the RLF-L-myc and the normal L-myc proteins is indistinguishable. '), ('9794', 'RET_PTC3', '', 'RET', 'PTC3', '16015630', '7', 'papillary carcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'Among the patients in these 3 age groups, the prevalence rate of RET/PTC1 was similar, but RET/PTC3 was observed most frequently among patients age < 20 years.     ///    \"When the tumors were grouped further according to histologic subtypes, the prevalence of RET/PTC3 was greater in solid/solid-follicular papillary carcinomas than in classic papillary carcinomas. \"'), ('9795', 'PAX3_FKHR', '', 'PAX3', 'FKHR', '15630526', '7', 'rhabdomyosarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Standard reverse transcriptase-polymerase chain reaction performed on RNA isolated from frozen sections showed 1 ARMS with a positivity for PAX3-FKHR with four patients classified as having ARMS and 1 as having spindle cell RMS were negative for both ARMS fusion transcripts (PAX3- and PAX7-FKHR). '), ('9796', 'DEK_CAN', 't(6;9)  / ', 'DEK', 'CAN', '1549122', '7', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'Sequence analysis of the dek-can cDNA showed that dek and can are merged without disruption of the original open reading frames and therefore the fusion mRNA encodes a chimeric DEK-CAN protein of 165 kDa. '), ('9797', 'RET_KIF5B', '', 'RET', 'KIF5B', '24133367', '7', 'non small cell lung cancer;lung cancer;adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'Two KIF5B-RET fusions and one CCDC6-RET fusion were identified. '), ('9798', 'SYT_SSX1', '', 'SYT', 'SSX1', '10685632', '7', 'synovial sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Three tumors had SYT-SSX2 fusion transcripts, whereas 19 had SYT-SSX1 phenotype. '), ('9799', 'MLL_DAB2IP', 't(9;11)  / t(9;11)(q34;q23) / ', 'MLL', 'DAB2IP', '14978793', '7', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', 'KB', '', 'As a result of the breakpoint in the AF9Q34-MLL fusion protein, this PH domain is disrupted. '), ('9800', 'CCDC6_RET', '', 'CCDC6', 'RET', '24133367', '7', 'non small cell lung cancer;lung cancer;adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Two KIF5B-RET fusions and one CCDC6-RET fusion were identified.'), ('9801', 'EWS_ERG', '', 'EWS', 'ERG', '9475198', '7', 'neuroectodermal tumor;ewing sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'This diagnosis was established by detection of EWS/ERG fusion transcript through reverse transcription polymerase chain reaction (RT-PCR) with nested primers. '), ('9802', 'SYT_SSX1', '', 'SYT', 'SSX1', '11274403', '7', '', 'PCR', '', '', '', '', '', '', '', 'To analyze the transcriptional regulation by SYT-SSX1, we established conditional expression system of SYT-SSX1 and examined the gene expression profiles.     ///    Deletion of the N-terminal 181 amino acids of SYT-SSX1 caused loss of its transforming activity.     ///    These data clearly demonstrate transforming activity of human oncogene SYT-SSX1 and also involvement of chromatin remodeling factor hBRM/hSNF2 alpha in human cancer..     ///    \"In this study, we have established 3Y1 rat fibroblast cell lines that constitutively express SYT, SSX1, and SYT-SSX1 and found that SYT-SSX1 promoted growth rate in culture, anchorage-independent growth in soft agar, and tumor formation in nude mice. \"    ///    Analysis of transforming activity of human synovial sarcoma-associated chimeric protein SYT-SSX1 bound to chromatin remodeling factor hBRM/hSNF2 alpha.. '), ('9803', 'ROS1_CD74', '', 'ROS1', 'CD74', '25157770', '7', '', '', 'Kinase', 'Oncogene', '', '', '', '', 'Seq', 'Acinar (including cribriform) and solid patterns were the two most common histologic subtypes in the ROS1 fusion tumors (7 of 12, 58.3%) and were predominantly seen in CD74-ROS1 fusion tumors (66.7%). '), ('9804', 'RGS17_IRA1', '', 'RGS17', 'IRA1', '15326299', '7', 'breast cancer\r\r', '', '', '', '', '', '', '', '', 'We have experimentally verified the presence of a previously unknown IRA1/RGS17 fusion in the breast cancer cell line MCF7. '), ('9805', 'FGFR3_TACC3', '', 'FGFR3', 'TACC3', '24452392', '7', 'squamous cell carcinoma;lung cancer\r\r', 'PCR;RT-PCR', 'Kinase', '', '', '', '', 'KB', 'Seq', 'We also examined 190 LCs for the FGFR3-TACC3 and FGFR3-BAIAP2L1 fusion transcripts using reverse transcription-polymerase chain reaction (RT-PCR) analysis.    ///    \"Although the expression of FGFR3-TACC3 and FGFR3-BAIAP2L1 fusion transcripts was not detected in any of the carcinomas, somatic FGFR3 mutations were detected in two (0.9%) LCs. \"'), ('9806', 'PDGFB_COL1A1', '', 'PDGFB', 'COL1A1', '10963386', '7', 'dermatofibrosarcoma protuberans;sarcoma\r\r', '', '', 'Oncogene', '', '', '', 'KB', '', 'A case of dermatofibrosarcoma protuberans of the vulva with a COL1A1/PDGFB fusion identical to a case of giant cell fibroblastoma..     ///    \"This is the first case of DFSP showing such a fusion point, which is intriguingly identical to that found in a GCF case, indicating that the COL1A1/PDGFB fusion point position does not seem to affect tumor morphology. \"'), ('9807', 'ETV6_NTRK3', 't(12;15)(p13;q25) / / ', 'ETV6', 'NTRK3', '10702799', '7', 'fibrosarcoma', '', 'Kinase', '', '', '', '', 'KB', 'Seq', 'Moreover, ETV6-NTRK3 has PTK activity and is autophosphorylated on tyrosine residues.'), ('9808', 'ETO_AML1', 't(8;21)(q22;q22) / t(3;21)(q26;q22) / t(3;21) / ', 'ETO', 'AML1', '8585955', '7', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'however, the chimeric AML1/ETO is a strong repressor of some AML1-dependent promoters. '), ('9809', 'JJAZ1_JAZF1', '', 'JJAZ1', 'JAZF1', '18772439', '7', '', '', '', '', '', '', '', '', '', 'The JAZF1-JJAZ1 RNA appears to arise from physiologically regulated trans-splicing between precursor messenger RNAs for JAZF1 and JJAZ1.     ///    \"We show that normal endometrial stromal cells contain a specific chimeric RNA joining 5\' exons of the JAZF1 gene on chromosome 7p15 to 3\' exons of the Polycomb group gene JJAZ1/SUZ12 on chromosome 17q11 and that this RNA is translated into JAZF1-JJAZ1, a protein with anti-apoptotic activity.\"    ///    \"We show that normal endometrial stromal cells contain a specific chimeric RNA joining 5\' exons of the JAZF1 gene on chromosome 7p15 to 3\' exons of the Polycomb group gene JJAZ1/SUZ12 on chromosome 17q11 and that this RNA is translated into JAZF1-JJAZ1, a protein with anti-apoptotic activity. \"'), ('9810', 'ETO_AML1', 't(11;17)(q23;q21) / t(15;17) / t(11;17)  / t(5;17)  / ', 'ETO', 'AML1', '15748426', '6', 'acute myeloid leukemia;chronic myeloid leukemia;acute promyelocytic leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'In acute myeloid leukemia M(2b), using new target therapy degradating AML1-ETO fusion protein and reducing the abnormal tyrosine kinase activity of c-kit will also lead to new therapeutic management in acute leukemias.. '), ('9811', 'MAML2_CRTC1', '', 'MAML2', 'CRTC1', '19827123', '5', 'mucoepidermoid carcinoma', 'PCR', '', '', '', '', 'Transcription_Factor', 'KB', 'Seq', 'To identify additional genetic alterations that might cooperate with CRTC1-MAML2 to promote disease progression, we performed a pilot high-resolution oligonucleotide array CGH (aCGH) and PCR-based genotyping study on 23 MEC samples including 14 fusion-positive samples for which we had clinical outcome information.     ///    \"While these analyses suggested that detection of CRTC1-MAML2 serves as a useful prognostic biomarker, we recently identified outlier cases of fusion-positive MEC associated with advanced-staged lethal disease. \"    ///    Prospective studies with larger case series will be needed to confirm that combined CRTC1-MAML2 and CDKN2A genotyping will optimally stage this disease..     ///    Unfavorable prognosis of CRTC1-MAML2 positive mucoepidermoid tumors with CDKN2A deletions..     ///     The CRTC1-MAML2 fusion oncogene underlies the etiology of mucoepidermoid salivary gland carcinoma (MEC) where it confers a favorable survival outcome as compared with fusion-negative MEC. '), ('9812', 'PAX3_FOXO1', '', 'PAX3', 'FOXO1', '23733015', '5', 'rhabdomyosarcoma;sarcoma\r\r', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', 'KB', 'Seq', 'Most ARMS express the PAX3-FOXO1 (P3F) fusion oncoprotein generated by the 2;13?chromosomal translocation.     ///    Identification of target genes of PAX3-FOXO1 in alveolar rhabdomyosarcoma.    ///    Identification of target genes of PAX3-FOXO1 in alveolar rhabdomyosarcoma.. '), ('9813', 'EML4_ALK', '', 'EML4', 'ALK', '23157740', '5', 'lung cancer;adenocarcinoma\r\r', 'PCR', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Based on the 2004 WHO classification, mutations of KRAS (P = 0.002) and EML4-ALK (P = 0.000), rather than EGFR (P = 0.502), showed significant differences among different subtypes.    ///    \"However, there was no association between TTF-1 expression and EML4-ALK fusions (P = 0.274).\"    ///    \"Mutations of epidermal growth factor receptor (EGFR) 18-21 exons (E18-21), KRAS 12/13 codons and EML4-ALK fusion in 212 cases of lung adenocarcinoma which underwent complete tumor resection, were detected by immunohistochemistry, PCR-amplifying and gene sequencing.\"    ///    \"Based on the 2004 WHO classification, mutations of KRAS (P = 0.002) and EML4-ALK (P = 0.000), rather than EGFR (P = 0.502), showed significant differences among different subtypes. \"    ///    \"The new classification, combined with TTF-1 immunomarker, can help to predict the molecular alterations of EGFR and KRAS genes, but can not indicate the EML4-ALK fusion in lung adenocarcinoma. \"    ///    \"Mutations of epidermal growth factor receptor (EGFR) 18-21 exons (E18-21), KRAS 12/13 codons and EML4-ALK fusion in 212 cases of lung adenocarcinoma which underwent complete tumor resection, were detected by immunohistochemistry, PCR-amplifying and gene sequencing. \"    ///    \"EML4-ALK fusions were most frequently found in the solid predominant with mucin production subtype (15.4%, 6/39), followed by colloid predominant adenocarcinoma (1/7), and no significant difference of EML4-ALK fusions was found among different histological subtypes (P = 0.181). \"    ///    \"EML4-ALK fusions were found in 6.1% of lung adenocarcinoma, the most common fusion mutation was type V1 (E13. \"    ///    \"However, there was no association between TTF-1 expression and EML4-ALK fusions (P = 0.274). \"'), ('9814', 'NUP107_LGR5', '', 'NUP107', 'LGR5', '22034177', '5', 'chondrosarcoma;liposarcoma;sarcoma\r\r', 'FISH;PCR;RT-PCR ', '', '', '', 'Receptor', '', 'KB', '', 'We also identified a NUP107-LGR5 fusion in a dedifferentiated liposarcoma but analysis of 17 additional samples did not confirm it as a recurrent event in this sarcoma type. '), ('9815', 'TCF3_PBX1', '', 'TCF3', 'PBX1', '26266519', '5', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia\r\r', 'FISH;PCR;RT-PCR ', '', '', '', '', 'Transcription_Factor', 'KB', 'Seq', 'TCF3-PBX1 (2.1?%) was associated with inferior outcome and higher central nervous system (CNS) relapse risk.     ///    \"The most common FOs are BCR-ABL, MLL-AF4, ETV6-RUNX1, and TCF3-PBX1, all of which have important prognostic and drug selection implications. \"    ///    \"The most common FOs are BCR-ABL, MLL-AF4, ETV6-RUNX1, and TCF3-PBX1, all of which have important prognostic and drug selection implications.\"'), ('9816', 'TFE3_ASPCR1', '', 'TFE3', 'ASPCR1', '18713311', '5', 'alveolar soft part sarcoma;brain edema', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'At the molecular level RT-PCR and sequencing analysis demonstrated ASPCR1-TFE3 fusion confirming the histological diagnosis of ASPS.     ///    Meningeal alveolar soft part sarcoma confirmed by characteristic ASPCR1-TFE3 fusion.. '), ('9817', 'EML4_ALK', '', 'EML4', 'ALK', '26104888', '5', 'non small cell lung cancer;lung cancer\r\r', 'PCR;RT-PCR', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Furthermore, the gene mutation frequency of EML4-ALK in the resistant cells was significantly higher than that in the parent cells.    ///    \"Furthermore, the gene mutation frequency of EML4-ALK in the resistant cells was significantly higher than that in the parent cells. \"    ///    The echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) expression was evaluated by RT-PCR and Western blot.     ///    Full-length sequencing method was used to compare the EML4-ALK genes in the parent and drug-resistant cells and analyze the mechanisms of drug resistance. '), ('9818', 'FLI_EWS', '', 'FLI', 'EWS', '18927503', '5', 'ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Most cases harbor the (11;22) (q24;q12) chromosomal translocation that encodes the EWS/FLI oncoprotein.     ///    \"The observation of microsatellites as transcriptional response elements for EWS/FLI suggest that these elements may not be \"\"junk\"\" after all.. \"    ///    EWS/FLI is an aberrant ETS-type transcription factor that dysregulates a number of genes important in the development of Ewing\'s sarcoma.     ///    \"Because EWS/FLI is the key oncoprotein in this tumor and ETS proteins are often dysregulated in various human cancers, Ewing\'s sarcoma serves as a useful paradigm for ETS-mediated oncogenesis. \"    ///    \"Microsatellites are EWS/FLI response elements: genomic \"\"junk\"\" is EWS/FLI\'s treasure.. \"    ///    \"We recently showed that EWS/FLI interacts with GGAA-microsatellites to regulate some of its target genes, including NR0B1, an EWS/FLI-regulated gene that is required for the oncogenic phenotype of Ewing\'s sarcoma. \"'), ('9819', 'EML4_ALK', '', 'EML4', 'ALK', '22768234', '5', 'non small cell lung cancer;squamous cell carcinoma', 'PCR', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'In a subgroup of non-smokers with adenocarcinoma, EGFR was the most frequently altered gene, with a mutation rate of 49.8%, followed by EML4-ALK (9.3%), PTEN (9.1%), PIK3CA (5.2%), c-Met (4.8%), KRAS (4.5%), STK11 (2.7%), and BRAF (1.9%). '), ('9820', 'MLL_LARG', '', 'MLL', 'LARG', '10681437', '5', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'Transcriptional orientation of both genes at 11q23 is from centromere to telomere, consistent with other data that suggest the MLL-LARG fusion resulted from an interstitial deletion rather than a balanced translocation. '), ('9821', 'TMPRSS2_ERG', '', 'TMPRSS2', 'ERG', '26294063', '5', 'prostate cancer;prostatic intraepithelial neoplasia\r\r', 'PCR', '', '', '', '', '', 'KB', 'Seq', 'ERG protein expression was limited to areas of TMPRSS2-ERG mRNA expression, but did not identify all of them.    ///    \" PCA3 and TMPRSS2-ERG are commonly overexpressed biomarkers in prostate cancer, but reports have emerged demonstrating altered expression also in areas outside the tumour foci in cancerous prostates. \"    ///    TMPRSS2-ERG mRNAs were detected in three patients and in 15 tissue samples in total.     ///    \"ERG protein expression was limited to areas of TMPRSS2-ERG mRNA expression, but did not identify all of them. \"    ///    \"TMPRSS2-ERG expression was detected in carcinoma foci, regions next to them, and in samples not adjacent to carcinoma foci. \"    ///    \"Altered PCA3 and TMPRSS2-ERG expression in histologically benign regions of cancerous prostates: a systematic, quantitative mRNA analysis in five prostates.. \"    ///    \"Our aim was to measure PCA3 and TMPRSS2-ERG expression systematically in all regions of prostate cross-sections, matching the data to corresponding tissue morphology. \"    ///    TMPRSS2-ERG and PCA3 mRNA levels were measured with quantitative reverse-transcription PCR assays in 270 samples from cross-sections of five radical prostatectomy specimens. '), ('9822', 'PAX3_FOXO1', '', 'PAX3', 'FOXO1', '19904978', '5', 'rhabdomyosarcoma;sarcoma\r\r', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', 'KB', 'Seq', 'Finally, we show that Pax3-FOXO1 is phosphorylated at Ser205 in a variety of translocation-containing ARMS cell lines.'), ('9823', 'FGFR3_TACC3', '', 'FGFR3', 'TACC3', '24850843', '5', 'non small cell lung cancer;lung cancer\r\r', 'PCR;RT-PCR', 'Kinase', '', '', '', '', 'KB', 'Seq', 'Of 1,328 tumors screened, two (0.2%) were BAG4-FGFR1 fusion and 15 (1.1%) were FGFR3-TACC3 fusion.    ///    \"Of 1,328 tumors screened, two (0.2%) were BAG4-FGFR1 fusion and 15 (1.1%) were FGFR3-TACC3 fusion. \"    ///    \"Six of 1,016 patients with lung adenocarcinoma were FGFR3-TACC3 fusions and 11 of 312 lung squamous cell carcinoma harbored BAG4-FGFR1 or FGFR3-TACC3 fusions. \"'), ('9824', 'KIF5B_RET', '', 'KIF5B', 'RET', '25047660', '5', 'lung cancer\r\r', 'PCR;RT-PCR', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'We aimed to provide a basis for the further development of the therapy for KIF5B-RET positive lung cancer patients.    ///    RT-PCR was used to screen for KIF5B-RET fusions in Chinese lung cancer patients.    ///    \"To verify the oncogenic activity of KIF5B-RET kinase in lung cancer cells, we manipulated its expression genetically followed by colony formation and tumor formation assays. \"    ///    \"Our data suggest that KIF5B-RET promotes the cell growth and tumorigenicity of non-small cell lung cancers through multilevel activation of STAT3 signaling, providing possible strategies for the treatment of KIF5B-RET positive lung cancers.. \"    ///    \"The mechanism by which KIF5B-RET kinase induces proliferation was investigated by western blot, coimmunoprecipitation, and administration of RET, MAPK and STAT3 inhibitors. \"    ///    \"In this study, we verified the oncogenic activity of KIF5B-RET fusion and investigated how KIF5B-RET activates the specific signaling pathways for cellular transformation. \"    ///    Our study identified a KIF5B-RET fusion in Chinese NSCLC patients and demonstrated that KIF5B-RET transfected cells showed a significantly increased proliferation rate and colony-forming ability.     ///    KIF5B-RET fusion is an oncogene identified in non-small cell lung cancers.     ///    KIF5B-RET fusion kinase promotes cell growth by multilevel activation of STAT3 in lung cancer.. ');
INSERT INTO `ChimerPub_dump` VALUES ('9825', 'ETS2_TMPRSS2', '', 'ETS2', 'TMPRSS2', '26817504', '5', 'prostate cancer\r\r', '', '', '', '', '', '', '', '', 'Given their antioxidant properties, we hypothesized that lycopene and tomato sauce may be especially protective against diseases harboring the common gene fusion transmembrane protease, serine 2 (TMPRSS2):v-ets avian erythroblastosis virus E26 oncogene homolog (ERG).     ///    TMPRSS2:ERG was assessed by ERG immunohistochemistry on tumor tissue microarrays constructed from radical prostatectomy specimens.    ///    Our results lend some support to the hypothesis that prostate cancers that harbor TMPRSS2:ERG may be etiologically distinct from fusion-negative cancers.     ///    \"In particular, tomato sauce consumption may play a role in reducing TMPRSS2:ERG-positive disease.. \"'), ('9826', 'TCRB_MYB', 't(6;7)(q23;q34) / ', 'TCRB', 'MYB', '17452517', '5', 'T ALL;T cell leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'Expression analysis, including allele-specific approaches, showed stronger C-MYB expression in the MYB-rearranged cases compared with other T-ALLs, and a dramatically skewed C-MYB allele expression in the TCRB-MYB cases, which suggests that a translocation-driven deregulated expression may overcome a cellular attempt to down-regulate C-MYB.     ///    \"Strikingly, profiling of the T-ALLs by clinical, genomic, and large-scale gene expression analyses shows that the TCRB-MYB translocation defines a new T-ALL subtype associated with a very young age for T-cell leukemia (median, 2.2 years) and with a proliferation/mitosis expression signature. \"'), ('9827', 'EML4_ALK', '', 'EML4', 'ALK', '25735977', '5', 'non small cell lung cancer;non small cell lung cancer;small cell lung c\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Thus, inhibition of ERK signaling pathway could be a potential strategy in treatment of NSCLC patients with EML4-ALK translocation..    ///    \"Thus, inhibition of ERK signaling pathway could be a potential strategy in treatment of NSCLC patients with EML4-ALK translocation.. \"    ///    \"Here, for the first time, we showed that H1299 NSCLC cells stably expressing EML4-ALK acquire EMT phenotype, associated with enhanced invasive migration and increased expression of EMT-inducing transcription factors. \"    ///    \"However, the role of EML4-ALK in malignant transformation is not entirely clear.\"    ///    EML4-ALK induces epithelial-mesenchymal transition consistent with cancer stem cell properties in H1299 non-small cell lung cancer cells..     ///    \"Moreover, we found that inhibition of ERK1/2 reversed EMT induced by EML4-ALK in H1299 cells. \"    ///    \"However, the role of EML4-ALK in malignant transformation is not entirely clear. \"    ///    \"Taken together, these results suggested that EML4-ALK induced ERK activation is mechanistically associated with EMT phenotype. \"'), ('9828', 'KIAA1549_BRAF', '', 'KIAA1549', 'BRAF', '19373855', '5', 'pilocytic astrocytoma\r\r', 'PCR', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'PCR and sequencing confirmed the presence of five KIAA1549-BRAF fusion variants, along with a single fusion between SRGAP3 and RAF1. '), ('9829', 'SYT_SSX4', '', 'SYT', 'SSX4', '11368913', '5', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Cloning and characterization of spliced fusion transcript variants of synovial sarcoma: SYT/SSX4, SYT/SSX4v, and SYT/SSX2v.     ///    Stable transfection of an SYT/SSX4 expression vector into human and murine cell lines correlated with a down-regulation of SYT transcripts.     ///    This was also observed in a synovial sarcoma tumor expressing SYT/SSX4.     ///    \"In the present investigation we cloned and sequenced the full-length cDNA of SYT/SSX1, SYT/SSX2 and SYT/SSX4 from synovial sarcoma tissues. \"    ///    The SYT/SSX4 and SYT/SSX2 open reading frame also differed from previously reported SYT/SSX sequences by an in-frame addition of 93bp exon located in the junction between exon 7 and 8 of the SYT. '), ('9830', 'SYT_SSX', '', 'SYT', 'SSX', '16227627', '5', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', ' The proto-oncoprotein SYT is involved in the unique translocation t(X;18) found in synovial sarcoma SYT-SSX fusions. '), ('9831', 'BCR_ABL1', '', 'BCR', 'ABL1', '15254401', '5', 'leukemia\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Unexpectedly, B cell precursor leukemia cells harboring a BCR-ABL1 gene rearrangement do not depend on antigen receptor mediated survival signals.     ///    \"However, upon inhibition of the BCR-ABL1 kinase activity by STI571, only leukemia cells expressing an antigen receptor are able to survive. \"    ///    \"Since resistance to STI571 is frequent in the therapy of BCR-ABL1(+) B cell precursor leukemia, antigen receptor signaling may represent a mechanism through which these cells can temporarily evade STI571-induced apoptosis. \"    ///    Interference of BCR-ABL1 kinase activity with antigen receptor signaling in B cell precursor leukemia cells.. '), ('9832', 'EWS_ERG', '', 'EWS', 'ERG', '15628889', '5', 'ewing sarcoma;neuroectodermal tumor;sarcoma\r\r', '', '', '', '', '', '', '', '', 'A multiplex real-time polymerase chain reaction assay detected an EWS-ERG fusion. '), ('9833', 'NUP98_HOXA9', '', 'NUP98', 'HOXA9', '11369863', '5', 'leukemia\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', 'Seq', 'Several human leukemias have been associated with a chromosomal translocation involving either the Hox gene (i.e., NUP98/HOXA9) or the gene encoding Pbx1 (E2A/PBX1). '), ('9834', 'EML4_ALK', '', 'EML4', 'ALK', '21502504', '5', 'non small cell lung cancer;lung cancer\r\r', 'PCR', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Cells resistant to higher doses (1 ?M) also developed a gatekeeper mutation, L1196M, within the kinase domain, rendering EML4-ALK insensitive to crizotinib.    ///    Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK.    ///    \"Cells resistant to higher doses (1 ?M) also developed a gatekeeper mutation, L1196M, within the kinase domain, rendering EML4-ALK insensitive to crizotinib. \"    ///    We found that cells resistant to intermediate doses of crizotinib developed amplification of the EML4-ALK gene.     ///    \"Although crizotinib was ineffectual against EML4-ALK harboring the gatekeeper mutation, we observed that two structurally different ALK inhibitors, NVP-TAE684 and AP26113, were highly active against the resistant cancer cells in vitro and in vivo. \"    ///    Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK.. '), ('9835', 'ETO_AML1', '', 'ETO', 'AML1', '16620548', '5', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'WT1 and AML1-ETO levels were normalized by internal control ABL gene.     ///    \"All correlation co-efficiencies were over 0.99 for WT1, AML1-ETO and ABL standard curves. \"    ///    Sixty-two AML samples were also detected AML1-ETO mRNA expression by RQ-PCR.     ///    \"There was an excellent correlation between WT1 and AML1-ETO gene expression levels (r = 0.88, P < 0.001). \"    ///    Simultaneously follow-up of WT1 and AML1-ETO levels were carried out in 50 samples from 8 AML patients. '), ('9836', 'EML4_ALK', '', 'EML4', 'ALK', '22843788', '4', 'non small cell lung cancer;lung cancer\r\r', 'PCR', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The expression of EML4-ALK was reduced at the transcriptional level, whereas phosphorylation of epidermal growth factor receptor (EGFR), HER2, and HER3 was upregulated, in H3122/TR cells compared with those in H3122 cells.    ///    \"The expression of EML4-ALK was reduced at the transcriptional level, whereas phosphorylation of epidermal growth factor receptor (EGFR), HER2, and HER3 was upregulated, in H3122/TR cells compared with those in H3122 cells. \"    ///    EGF-mediated activation of HER family signaling is associated with ALK-TKI resistance in lung cancer positive for EML4-ALK.. '), ('9837', 'FLI1_ERG', '', 'FLI1', 'ERG', '9836070', '4', 'ewing sarcoma', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Seventy-seven PB samples from 28 patients had EWS-FLI1/ERG transcripts.     ///    \"The presence of specific EWS-FLI1 or EWS-ERG transcripts in peripheral blood (PB) samples of patients being treated for ET was prospectively evaluated, and these data were correlated to their clinical status. \"'), ('9838', 'FUS_DDIT3', '', 'FUS', 'DDIT3', '20515481', '4', 'liposarcoma;sarcoma\r\r', 'PCR', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', 'Seq', ' The FUS-DDIT3 fusion oncogene encodes an abnormal transcription factor that has a causative role in the development of myxoid/round-cell liposarcomas (MLS/RCLS).     ///    FLT1 expression was dramatically increased in transfected cells stably expressing FUS-DDIT3 and present at high levels in cell lines derived from MLS.    ///    Nuclear expression of FLT1 and its ligand PGF in FUS-DDIT3 carrying myxoid liposarcomas suggests the existence of an intracrine signaling loop.    ///    Nuclear expression of FLT1 and its ligand PGF in FUS-DDIT3 carrying myxoid liposarcomas suggests the existence of an intracrine signaling loop..     ///    We have previously identified FLT1 (VEGFR1) as a candidate downstream target gene of FUS-DDIT3.     ///    Our results imply that FLT1 is induced as an indirect downstream effect of FUS-DDIT3 expression in MLS.     ///    This could be a consequence of the ability of FUS-DDIT3 to hijack parts of normal adipose tissue development and reprogram primary cells to a liposarcoma-like phenotype. '), ('9839', 'TMPRSS2_ERG', '', 'TMPRSS2', 'ERG', '18676740', '4', 'prostate cancer\r\r', 'PCR', '', '', '', '', '', 'KB', 'Seq', 'Copy numbers of TMPRSS2-ERG splice variants were determined by quantitative reverse transcription-PCR in laser capture microdissected prostate cancer cells.     ///    Full-length TMPRSS2-ERG transcripts were cloned and sequenced from a cDNA library generated from pooled RNA of six TMPRSS2-ERG fusion-positive prostate tumors.     ///    This study focuses on qualitative and quantitative features of full-length TMPRSS2-ERG transcripts in prostate cancer.     ///    \"Two types of TMPRSS2-ERG cDNAs were identified: type I, which encodes full-length prototypical ERG protein (ERG1, ERG2, ERG3), and type II, encoding truncated ERG proteins lacking the ETS domain (ERG8 and a new variant, TEPC). \"    ///    Delineation of TMPRSS2-ERG splice variants in prostate cancer.. '), ('9840', 'MSN_ALK', '', 'MSN', 'ALK', '11310834', '4', 'anaplastic large cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Molecular characterization of a new ALK translocation involving moesin (MSN-ALK) in anaplastic large cell lymphoma..     ///    The hybrid MSN-ALK protein had a molecular weight of 125 kd and contained an active tyrosine kinase domain. '), ('9841', 'TMPRSS2_ERG', '', 'TMPRSS2', 'ERG', '25007891', '4', 'prostate cancer\r\r', 'PCR', '', '', '', '', '', 'KB', 'Seq', 'Three tissue microarrays (TMAs) containing samples from 98 patients with PCa and one TMA of 27 samples from individuals without PCa were tested for ERG immunostaining, and the presence of TMPRSS2:ERG transcripts was confirmed by quantitative real time PCR (qRT-PCR).    ///    \"Three tissue microarrays (TMAs) containing samples from 98 patients with PCa and one TMA of 27 samples from individuals without PCa were tested for ERG immunostaining, and the presence of TMPRSS2:ERG transcripts was confirmed by quantitative real time PCR (qRT-PCR). \"    ///    The role of TMPRSS2:ERG in molecular stratification of PCa and its association with tumor aggressiveness: a study in Brazilian patients.. '), ('9842', 'MLL_ENL', '', 'MLL', 'ENL', '12651265', '4', 'acute lymphoblastic leukemia;T ALL;lymphoblastic leukemia;leukemia\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'In this study we adapted the multiplex RT-PCR assay, previously described by Pallisgaard et al., to detect all the most frequent genetic lesions with their characteristic splicing variants occurring in acute lymphoblastic leukemia, such as the MLL/AF4, MLL/ENL, BCR/ABL p190 (e1a2) and p210 (b2a2,b3a2) isoforms, E2A/PBX1, TEL/AML1, SIL/TAL1 and the novel NUP98/RAP1GDS1 transcript, recently described in a T-ALL leukemic subtype. '), ('9843', 'BCR_ABL1', '', 'BCR', 'ABL1', '18268888', '4', 'leukemia\r\r', 'PCR;RT-PCR', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', ' RT-PCR studies in 93 patients with chronic myelogenous leukemia from the Mexican West were done in order to know the proportion of b2a2 and b3a2 BCR/ABL1 transcripts.     ///    Prevalence of the BCR/ABL1 transcripts in Mexican patients with chronic myelogenous leukemia.. '), ('9844', 'PAX3_FKHR', '', 'PAX3', 'FKHR', '9490279', '4', 'small cell sarcoma', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'This biphenotypic tumor showed simultaneous expression of EWS-FLI1 and PAX3-FKHR transcripts, specific of Ewing family tumors and alveolar rhabdomyosarcoma, respectively. '), ('9845', 'BCR_ABL1', '', 'BCR', 'ABL1', '22937329', '4', 'chronic myeloid leukemia;myeloid leukemia;leukemia\r\r', 'PCR', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', ' While most patients with chronic myeloid leukemia (CML) express either e13a2 or e14a2 BCR-ABL1 transcripts, a significant minority expresses variant transcripts, of which e19a2 is the most common.     ///    \"Although considered to have a relatively favourable outcome, reported responses to tyrosine kinase inhibitor (TKI) therapy are variable with molecular monitoring in CML patients with e19a2 BCR-ABL1 transcripts rarely reported. \"    ///    Chronic Myeloid Leukemia with e19a2 BCR-ABL1 Transcripts and Marked Thrombocytosis: The Role of Molecular Monitoring..     ///    This case serves to demonstrate the requirement for prospective real-time quantitative PCR (RQ-PCR) assays for patients with variant BCR-ABL1 transcript types and standardisation of such assays to enable modern patient management..     ///    \"A case of e19a2 BCR-ABL1 CML with marked thrombocytosis is described in which the value of molecular monitoring is emphasised during treatment interruptions, dose reductions, and changes. \"'), ('9846', 'RET_PTC3', '', 'RET', 'PTC3', '9001272', '4', 'hashimoto thyroiditis', 'PCR;RT-PCR', 'Kinase', 'Oncogene', '', '', '', '', '', 'Using a sensitive and specific reverse transcriptase-polymerase chain reaction (RT-PCR) assay, we found messenger RNA (mRNA) expression for the RET/PTC1 and RET/PTC3 oncogenes in 95% of the Hashimoto\'s patients studied.     ///    The newly identified oncogenes RET/PTC1 and RET/PTC3 provide useful and specific markers of the early stages of papillary carcinoma as they are highly specific for malignant cells. '), ('9847', 'NRG1_CD74', '', 'NRG1', 'CD74', '24913807', '4', 'mucinous carcinoma;non small cell lung cancer', '', '', '', '', '', '', '', '', 'Multidriver mutation analysis in pulmonary mucinous adenocarcinoma in Taiwan: identification of a rare CD74-NRG1 translocation case..     ///    Patients harboring CD74-NRG1 positive tumors may present with uncommon imaging features..     ///    \"Using the direct RNA sequencing method, we discovered a rare CD74-NRG1 fusion (8 %), an echinoderm microtubule-associated protein like 4 (EML4)-ALK fusion (17 %), and three KRAS mutations (25 %). \"    ///    The CD74-NRG1 fusion mutation is rare and may be exclusively present in patients with pulmonary mucinous adenocarcinoma.     ///    \"We did not detect any CD74-NRG1 fusion in the 109 adenocarcinoma of other subtypes, which were all negative for EGFR, KRAS, ALK, and ROS1. \"    ///    The rare CD74-NRG1 fusion positive patient presented with uncommon radiological features.     ///    \"We did not detect any CD74-NRG1 fusion in the 109 adenocarcinoma of other subtypes, which were all negative for EGFR, KRAS, ALK, and ROS1.\"'), ('9848', 'MLL_AF10', '', 'MLL', 'AF10', '9305618', '4', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Sequence analysis of the fusion region on the amplified cDNA fragment showed an in-frame joining of exon e5 of the MLL gene and position 1931 of the cDNA sequence of the AF10 gene, giving rise to a new MLL-AF10 transcript.     ///    A novel MLL-AF10 fusion mRNA variant in a patient with acute myeloid leukemia detected by a new asymmetric reverse transcription PCR method..     ///     A novel variant of the chimerical MLL-AF10 mRNA transcript was detected in a pediatric patient with acute myeloid leukemia (AML) by a new asymmetric reverse-transcription polymerase chain reaction (ART-PCR) method. '), ('9849', 'SLC45A3_ELK4', '', 'SLC45A3', 'ELK4', '21261984', '3', 'lung cancer;adenocarcinoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', 'KB', 'Seq', 'Expression of TICs correlates with that of the upstream gene, which can explain the prostate-specific pattern of some TIC events and the restriction of the SLC45A3-ELK4 e4-e2 TIC to ERG-negative prostate samples, as confirmed in 20 matched prostate tumor and normal samples and 9 lung cancer cell lines.    ///    \"Expression of TICs correlates with that of the upstream gene, which can explain the prostate-specific pattern of some TIC events and the restriction of the SLC45A3-ELK4 e4-e2 TIC to ERG-negative prostate samples, as confirmed in 20 matched prostate tumor and normal samples and 9 lung cancer cell lines. \"'), ('9850', 'SYT_SSX1', '', 'SYT', 'SSX1', '11064357', '3', 'histiocytoma;soft tissue sarcoma', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'There was a trend for biphasic synovial sarcoma to contain the SYT-SSX1 fusion. '), ('9851', 'ERG_ELF4', '', 'ERG', 'ELF4', '16303180', '3', 'acute myeloid leukemia;myeloid leukemia;leukemia;ewing sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'This is the first reported case of an ELF4-ERG fusion and identification of the specific ERG exon involved in the fusion that differentiates ERG isoforms. '), ('9852', 'PAX3_FOXO1', '', 'PAX3', 'FOXO1', '25821947', '3', 'rhabdomyosarcoma;sarcoma\r\r', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', 'KB', 'Seq', 'We found that inhibiting the phosphorylation of PAX3-FOXO1 at Ser201 significantly reduced migration, invasion and proliferation in two independent ARMS tumor cell lines.    ///    \"We found that inhibiting the phosphorylation of PAX3-FOXO1 at Ser201 significantly reduced migration, invasion and proliferation in two independent ARMS tumor cell lines. \"    ///    Inhibiting phosphorylation of the oncogenic PAX3-FOXO1 reduces alveolar rhabdomyosarcoma phenotypes identifying novel therapy options..     ///    \"These results identify phosphorylation of PAX3-FOXO1, especially at Ser201, as a novel biological target that can be explored as a promising avenue for ARMS therapies. \"    ///    \"Along these lines, we demonstrated that PAX3-FOXO1 is phosphorylated at three specific sites and that its pattern of phosphorylation is altered relative to wild-type Pax3 throughout early myogenesis and in ARMS tumor cells. \"    ///    \"Consistent with these in vitro results, we demonstrate for the first time that PAX3-FOXO1 is phosphorylated at Ser201 and Ser205 in a primary tumor sample and in tumor cells actively invading the surrounding normal tissue. \"    ///    This report is the first to demonstrate that the direct inhibition of PAX3-FOXO1 phosphorylation reduces ARMS tumor phenotypes in vitro and that these phosphorylation events are present in primary human ARMS tumors and invading tumor cells.     ///    \" Patients with translocation-positive alveolar rhabdomyosarcoma (ARMS), an aggressive childhood tumor primarily characterized by the PAX3-FOXO1 oncogenic fusion protein, have a poor prognosis because of lack of therapies that specifically target ARMS tumors. \"    ///    \"To address this gap in knowledge, we used small molecule inhibitors or mutational analysis to specifically inhibit phosphorylation of PAX3-FOXO1 to investigate how altering phosphorylation of the oncogenic fusion protein affects ARMS phenotypes.\"    ///    \"To address this gap in knowledge, we used small molecule inhibitors or mutational analysis to specifically inhibit phosphorylation of PAX3-FOXO1 to investigate how altering phosphorylation of the oncogenic fusion protein affects ARMS phenotypes. \"'), ('9853', 'EML4_ALK', '', 'EML4', 'ALK', '23683537', '3', 'non small cell lung cancer;lung cancer;adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', ' The coexistence of EGFR and ALK-EML4 gene mutations represents a rare event (about 1%) in patients with non small cell lung cancer (NSCLC) and the few cases described in the literature have all been treated by different methods. '), ('9854', 'BCR_ABL1', '', 'BCR', 'ABL1', '10615128', '3', '', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'One model uses the \'knock-in\' approach to induce leukaemia by p190 BCR-ABL1(ref.     ///    Reversibility of acute B-cell leukaemia induced by BCR-ABL1..     ///    \"The most common form, p210 BCR-ABL1, is found in more than 90% of patients with chronic myelogenous leukaemia (CML) and in up to 15% of adult patients with de novoacute lymphoblastic leukaemia (ALL). \"    ///    We have taken a new approach to determine if ablation of the genetic abnormality is sufficient for reversion by generating a conditional transgenic model of BCR-ABL1 (also known as BCR-ABL)-induced leukaemia. '), ('9855', 'DEK_CAN', '', 'DEK', 'CAN', '8895527', '3', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'This finding suggests that CC112 may contribute an essential function to the leukemogenic effect of DEK-CAN and SET-CAN..     ///     The recurrent chromosomal translocation (6;9) is associated with acute myeloid leukemia and results in expression of the DEK-CAN fusion protein.     ///    CC112 also interacts with the DEK-CAN and SET-CAN fusion proteins.     ///    \"Interaction of cellular proteins with the leukemia specific fusion proteins DEK-CAN and SET-CAN and their normal counterpart, the nucleoporin CAN.. \"'), ('9856', 'SET_CAN', '', 'SET', 'CAN', '8895527', '3', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'This finding suggests that CC112 may contribute an essential function to the leukemogenic effect of DEK-CAN and SET-CAN..     ///    CC112 also interacts with the DEK-CAN and SET-CAN fusion proteins.     ///    \"In much the same way, CAN is fused to SET in a patient with acute undifferentiated leukemia, producing a SET-CAN fusion protein. \"    ///    \"Interaction of cellular proteins with the leukemia specific fusion proteins DEK-CAN and SET-CAN and their normal counterpart, the nucleoporin CAN.. \"'), ('9857', 'SS18_SSX1', '', 'SS18', 'SSX1', '18234968', '3', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'Furthermore, SS18-SSX1 expression altered the induction of p53-regulated genes in response to cellular stress by abrogating the transactivation of HDM2, PUMA, and NOXA but not p21.    ///    \"Here, we show that SS18-SSX1 negatively regulates the stability of the tumor suppressor p53 under basal conditions.\"'), ('9858', 'MTG8_AML1', 't(8;21)  / ', 'MTG8', 'AML1', '8683993', '3', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'This translocation interrupts two genes, AML1 on chromosome 21q and MTG8 (ETO) on 8q to form a chimeric gene AML1/MTG8 on the der(8) chromosome. '), ('9859', 'PPARG_PAX8', '', 'PPARG', 'PAX8', '12170088', '3', 'hurthle cell tumors', 'PCR;RT-PCR', '', '', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'Most sporadic follicular carcinomas positive for PAX8-PPARgamma were overtly invasive, whereas tumors lacking the rearrangement were predominantly minimally invasive.     ///    The absence of PAX8-PPARgamma rearrangements in Hurthle cell tumors and papillary thyroid carcinomas highlights the differences in the molecular pathogenesis of these thyroid tumors..     ///    \" A PAX8-PPARgamma rearrangement has been recently identified in follicular thyroid carcinomas, but not in follicular adenomas or other thyroid tumors. \"    ///    PAX8-PPARgamma rearrangement in thyroid tumors: RT-PCR and immunohistochemical analyses..     ///    \"The two follicular adenomas positive for PAX8-PPARgamma had trabecular growth pattern and thick capsule, but no invasion, and thus may represent \"\"pre-invasive\"\" follicular carcinomas. \"    ///    \"PAX8-PPARgamma was detected by RT-PCR in eight of 15 (53%) follicular carcinomas and two of 25 (8%) follicular adenomas but not in 35 papillary carcinomas (including 12 follicular variants), 12 Hurthle cell carcinomas, 12 Hurthle cell adenomas, two anaplastic carcinomas, one poorly differentiated carcinoma, or 16 hyperplastic nodules. \"    ///    We report here the analyses of PAX8-PPARgamma in a series of 118 thyroid tumors using a newly developed RT-PCR assay to detect this rearrangement in frozen and paraffin-embedded tissues and using immunostaining with a PPARgamma antibody.     ///    \"Strong, diffuse nuclear immunostaining with the PPARgamma antibody correlated with the presence of PAX8-PPARgamma detected by RT-PCR. \"'), ('9860', 'ETO _AML1', '', 'ETO ', 'AML1', '17989718', '3', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'Here, we systematically showed that constitutively and overexpressed AML1-ETO protein was cleaved to four fragments of 70, 49, 40 and 25 kDa by activated caspase-3 during apoptosis induction by extrinsic mitochondrial and death receptor signaling pathways.     ///    \"When these two aspartates were mutated into alanines, more intriguingly, the apoptosis-amplified action of AML1-ETO induction completely disappeared, while inducible expression of the caspase-3-cleaved 70 kDa fragment of AML1-ETO after tetracycline removal is sufficient to enhance apoptotic sensitivity. \"    ///    Such dichotomous functions make it difficult to clarify the role of AML1-ETO in leukemogenesis.     ///    Site-directed mutagenesis analyses identified two nonclassical aspartates (TMPD188 and LLLD368) as caspase-3-targeted sites in the AML1-ETO sequence.     ///    The in vitro proteolytic system combined with MALDI-TOF/TOF mass spectrometer confirmed that AML1-ETO and wild-type ETO but not RUNX1 (AML1) proteins were direct substrates of apoptosis executioner caspase-3.     ///     Leukemia-associated fusion protein AML1-ETO is a product of the chromosome translocation (8;21) frequently occurred in acute myeloid leukemia (AML).     ///    Multi-sites cleavage of leukemogenic AML1-ETO fusion protein by caspase-3 and its contribution to increased apoptotic sensitivity.. '), ('9861', 'RET_HOOK3', '', 'RET', 'HOOK3', '17639057', '3', '', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'HOOK3-RET: a novel type of RET/PTC rearrangement in papillary thyroid carcinoma..     ///    \"Expression of the HOOK3-RET cDNA in NIH3T3 cells resulted in the formation of transformed foci and in tumor formation after injection into nude mice, confirming the oncogenic nature of HOOK3-RET.. \"    ///    \"A fusion product between exon 11 of HOOK3 and exon 12 of RET gene was identified by 5\'RACE, and the presence of chimeric HOOK3-RET protein of 88 kDa was detected by western blot analysis with an anti-RET antibody. \"'), ('9862', 'NPM_ALK', 't(2;5)  / ', 'NPM', 'ALK', '11110708', '3', 'anaplastic large cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'Here, we show that NPM-ALK recruits the C-terminal SH2 domain of the phosphatidylinositol 3-kinase (PI 3kinase) p85 subunit.     ///    \"Thus, NPM-ALK activates the antiapoptotic PI 3-kinase/Akt pathway, which likely contributes to the molecular pathogenesis of ALCL. \"    ///    \"Furthermore, apoptosis induced by overexpression of the proapoptotic molecule Bad could be partially blocked by the overexpression of NPM-ALK. \"    ///    We have previously identified PLC-gamma as a crucial downstream signaling molecule of NPM-ALK that contributes to its mitogenic potential.     ///    Primary murine bone marrow retrovirally transduced with NPM-ALK showed a transformed phenotype that was reversible on treatment with PI 3-kinase inhibitors. '), ('9863', 'EWS_ERG', '', 'EWS', 'ERG', '7530783', '3', 'rhabdomyosarcoma;desmoplastic small round cell tumor;ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'EWS-FLI1 or EWS-ERG fusions were detected in six of eight Ewing\'s sarcomas and one of seven undifferentiated sarcomas.     ///    \"These assays detect PAX3-FKHR and PAX7-FKHR chimeric transcripts in alveolar rhabdomyosarcoma, EWS-FLI1 and EWS-ERG chimeric transcripts in Ewing\'s sarcoma, and EWS-WT1 chimeric transcripts in desmoplastic small round cell tumor. \"'), ('9864', 'PAX3_FKHR', '', 'PAX3', 'FKHR', '7530783', '3', 'rhabdomyosarcoma;desmoplastic small round cell tumor;ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'PAX3-FKHR or PAX7-FKHR fusions were present in 18 of 21 alveolar rhabdomyosarcomas, two of 30 embryonal rhabdomyosarcomas, and one of seven undifferentiated sarcomas.     ///    \"These assays detect PAX3-FKHR and PAX7-FKHR chimeric transcripts in alveolar rhabdomyosarcoma, EWS-FLI1 and EWS-ERG chimeric transcripts in Ewing\'s sarcoma, and EWS-WT1 chimeric transcripts in desmoplastic small round cell tumor. \"'), ('9865', 'PAX7_FKHR', '', 'PAX7', 'FKHR', '7530783', '3', 'rhabdomyosarcoma;desmoplastic small round cell tumor;ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'PAX3-FKHR or PAX7-FKHR fusions were present in 18 of 21 alveolar rhabdomyosarcomas, two of 30 embryonal rhabdomyosarcomas, and one of seven undifferentiated sarcomas.     ///    \"These assays detect PAX3-FKHR and PAX7-FKHR chimeric transcripts in alveolar rhabdomyosarcoma, EWS-FLI1 and EWS-ERG chimeric transcripts in Ewing\'s sarcoma, and EWS-WT1 chimeric transcripts in desmoplastic small round cell tumor. \"'), ('9866', 'PSF_TFE3', '', 'PSF', 'TFE3', '12902986', '3', 'papillary renal cell carcinoma', '', '', '', '', '', '', '', '', 'Our results indicate that PSF-TFE3 acts through a novel mechanism, and exports TFE3, p53 and possibly other factors from the nucleus to the cytoplasm for degradation leading to the transformed phenotype.    ///    \"In UOK-145 papillary renal carcinoma cells, which endogenously express PSF-TFE3, siRNA complementary to the PSF-TFE3 fusion junction leads to a reduction in PSF-TFE3 and redistribution of endogenous TFE3 and p53 from the cytoplasmic compartment to the nucleus. \"    ///    \"Although PSF-TFE3 has no effect on the nuclear localization of wild-type PSF, it sequesters wild-type TFE3 as well as p53 in the extranuclear compartment leading to functionally null p53 and TFE3 cells. \"    ///    \"Thus, PSF-TFE3 is a promising target for the treatment for a subset of renal cell carcinomas.. \"    ///    PSF-TFE3 oncoprotein in papillary renal cell carcinoma inactivates TFE3 and p53 through cytoplasmic sequestration..     ///    \"Unlike wild-type TFE3 or PSF, which are nuclear proteins, PSF-TFE3 is not a nuclear protein and is targeted to the endosomal compartment. \"    ///    \"Our results indicate that PSF-TFE3 acts through a novel mechanism, and exports TFE3, p53 and possibly other factors from the nucleus to the cytoplasm for degradation leading to the transformed phenotype. \"    ///    \"In this study, we explored the role of PSF-TFE3 fusion protein in mediating cell transformation.\"    ///    \"In this study, we explored the role of PSF-TFE3 fusion protein in mediating cell transformation. \"'), ('9867', 'COL1A1_PDGFB', '', 'COL1A1', 'PDGFB', '23432099', '3', 'dermatofibrosarcoma protuberans;sarcoma\r\r', '', '', 'Oncogene', '', '', '', 'KB', 'Seq', 'Translocations in the COL1A1/PDGFB gene imply susceptibility to targeted treatment modalities for therapy-resistant cases..    ///    Translocations in the COL1A1/PDGFB gene imply susceptibility to targeted treatment modalities for therapy-resistant cases.. '), ('9868', 'CALM_AF10', '', 'CALM', 'AF10', '16921363', '3', 'T ALL\r\r', '', '', '', '', '', '', '', '', 'Here, we analysed the molecular mechanism of leukaemogenesis by CALM-AF10.     ///    Leukaemic transformation by CALM-AF10 involves upregulation of Hoxa5 by hDOT1L..     ///    We demonstrate that CALM-AF10 fusion is both necessary and sufficient for leukaemic transformation.     ///    \"Thus, our study establishes CALM-AF10 fusion as a cause of leukaemia and reveals that mistargeting of hDOT1L and upregulation of Hoxa5 through H3K79 methylation is the underlying mechanism behind leukaemia caused by CALM-AF10 fusion.. \"'), ('9869', 'ETO_AML1', 't(8;21)  / t(15;17)  / ', 'ETO', 'AML1', '18264136', '3', '', '', '', '', '', '', '', '', '', 'We discuss the relevance of GEM AML from embryonic stem cell-mediated (for example retinoic acid receptor-alpha fusions and AML1/ETO) models. '), ('9870', 'PTPRK_RSPO3', '', 'PTPRK', 'RSPO3', '26700806', '3', 'colorectal cancer', '', '', '', '', '', '', 'KB', 'Seq', 'Targeting PTPRK-RSPO3 colon tumours promotes differentiation and loss of stem-cell function.    ///    \"This observation, combined with functional assays, suggests that a stem-cell compartment drives PTPRK-RSPO3 colorectal tumour growth and indicates that the therapeutic targeting of stem-cell properties within tumours may be a clinically relevant approach for the treatment of colorectal tumours. \"    ///    Targeting PTPRK-RSPO3 colon tumours promotes differentiation and loss of stem-cell function.. '), ('9871', 'FUS_DDIT3', '', 'FUS', 'DDIT3', '20473880', '3', 'liposarcoma;sarcoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', 'Seq', 'Real-time polymerase chain reaction showed FUS-DDIT3 fusion in both components in five of eight cases in the absence (zero of five) of MDM2 and CDK4 amplification. '), ('9872', 'EML4_ALK', '', 'EML4', 'ALK', '22617245', '3', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'We selected NSCLC cell lines--A549 (KRAS G12S), NCI-H3255 (EGFR L858R), NCI-H3122 (EML4-ALK E13;A20), and HCC78 (SLC34A2-ROS1)-to evaluate the antiproliferative effects of submicromolar concentrations of the multitargeted TKIs imatinib, sorafenib, erlotinib, and crizotinib.    ///    \"We selected NSCLC cell lines--A549 (KRAS G12S), NCI-H3255 (EGFR L858R), NCI-H3122 (EML4-ALK E13;A20), and HCC78 (SLC34A2-ROS1)-to evaluate the antiproliferative effects of submicromolar concentrations of the multitargeted TKIs imatinib, sorafenib, erlotinib, and crizotinib. \"'), ('9873', 'RARA_PLZF', '', 'RARA', 'PLZF', '16331271', '3', 'acute promyelocytic leukemia;leukemia\r\r', '', '', 'Oncogene', '', 'Receptor', 'Transcription_Factor', '', '', 'Similarly to what was observed in human APL patients, we found that NPM/RAR alpha and PML/RAR alpha, but not PLZF/RAR alpha leukemia, was responsive to all-trans retinoic acid (ATRA) or As2O3 treatments.     ///    \"Similarly, hCG-PLZF/RAR alpha TM displayed a different phenotype where terminally differentiated myeloid cells predominated. \"    ///    \"Leukemia with distinct phenotypes in transgenic mice expressing PML/RAR alpha, PLZF/RAR alpha or NPM/RAR alpha.. \"    ///    \"Importantly, the NPM/RAR alpha oncoprotein was found to localize in the nucleolus, unlike PML/RAR alpha and PLZF/RAR alpha, thus possibly interfering with the normal function of NPM. \"    ///    We compared the features of the leukemia observed in these TM with those in hCG-PML/RAR alpha and hCG-PLZF/RAR alpha TM. '), ('9874', 'SYT_SSX2', '', 'SYT', 'SSX2', '11866985', '3', 'synovial sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'A specific SYT-SSX RT-PCR product was found in 19 of 20 (95%) synovial sarcomas tested and of the 13 tumors containing SYT-SSX2, 10 were monophasic. '), ('9875', 'ETV6_NTRK3', '', 'ETV6', 'NTRK3', '15659957', '3', 'synovial sarcoma;ewing sarcoma;chronic myeloid leukemia;myeloid leukemia;leukemia;sarcoma\r\r', '', 'Kinase', '', '', '', '', 'KB', 'Seq', 'Functional knowledge of ETV6-NTRK3 has advanced so that strategies for screening small molecule inhibitors can proceed.    ///    Functional knowledge of ETV6-NTRK3 has advanced so that strategies for screening small molecule inhibitors can proceed. '), ('9876', 'PBX1_E2A', 't(1;19) / t(1;19)  / ', 'PBX1', 'E2A', '9108411', '2', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia;lymphoma\r\r', '', '', '', '', '', 'Transcription_Factor', '', '', 'The obtained antibodies recognize specifically the chimeric E2A/pbx1 fusion protein and lack cross-reactivities with E2A and pbx1. '), ('9877', 'SYT_SSX2', '', 'SYT', 'SSX2', '18563504', '2', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'These mice develop synovial sarcoma when SYT-SSX2 is expressed within myoblasts, thereby identifying a source of this enigmatic tumor and establishing a mouse model of this disease that recapitulates the clinical, histologic, immunohistochemical, and transcriptional profile of human synovial sarcomas. '), ('9878', 'PAX3_FKHR', '', 'PAX3', 'FKHR', '15184910', '2', 'rhabdomyosarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'In the presence of cycloheximide, CXCR4 and PAX3 are still inducible, supporting the hypothesis that these genes are direct transcriptional targets of PAX3-FKHR.     ///    These findings of genes regulated by PAX3-FKHR will direct future biological and clinical investigation to important pathways contributing to ARMS tumorigenesis and progression..     ///    This inducible system permits short-term evaluation of downstream expression targets of PAX3-FKHR and complements a panel of stable long-term RD subclones constitutively expressing PAX3-FKHR.     ///    \"Using these two sets of resources, we investigated several candidate PAX3-FKHR target genes. \"    ///    \"First, we demonstrated in both short-term and long-term systems that PAX3-FKHR upregulates expression of the gene encoding the chemokine receptor CXCR4. \"    ///    \"In addition, we found that expression of wild-type PAX3 is upregulated, whereas expression of wild-type PAX7 is downregulated by PAX3-FKHR. \"    ///    \"To explore molecular pathways altered by this oncoprotein, we generated an inducible form by fusing PAX3-FKHR to a modified estrogen receptor ligand-binding domain and expressed this construct in the RD embryonal rhabdomyosarcoma cell line. \"    ///    \"Inducible short-term and stable long-term cell culture systems reveal that the PAX3-FKHR fusion oncoprotein regulates CXCR4, PAX3, and PAX7 expression.. \"'), ('9879', 'PAX3_FKHR', '', 'PAX3', 'FKHR', '12414908', '2', 'rhabdomyosarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Coexpression of PAX3/FKHR increased basal transcriptional activity from a GLUT4 promoter reporter (GLUT4-P) in C2C12, SaOS-2, and Chinese hamster ovary-K1 cells in a dose-dependent and tissue-specific manner.     ///    \"PAX3/FKHR mutants with deletions in either the homeodomain (DeltaHD) or the FKHR-derived activation domain (DeltaFKHR), or in which the PAX3-derived paired domain (PD) was point-mutated (PD-R56L), were unable to activate GLUT4-P. \"    ///    \"Thus, the functional interaction of PAX3/FKHR with GLUT4-P appears to require all of the functional domains of PAX3/FKHR, as well as a -4/+36-bp region within the GLUT4 promoter. \"    ///    \"Therefore, we evaluated the role of PAX3/FKHR in the regulation of GLUT4 gene expression in muscle tumorigenesis. \"    ///    \"EMSA studies established that the PAX3/FKHR protein directly and specifically binds to this region and to a shorter fragment, -4/+36 bp, that contains potential binding sites for HD and PD, but not to a -4/+36-bp fragment whose HD and PD sites have been mutated. \"    ///    \"Taken together, the data suggest that the GLUT4 gene is a downstream target of PAX3/FKHR and that GLUT4 is aberrantly transactivated by this oncoprotein both in vivo and in vitro.. \"    ///    \"GLUT4 mRNA and protein were detected in ARMS-derived human biopsies and in ARMS-derived RH30 myoblasts, which both express the PAX3/FKHR chimeric protein, but not in either C2C12 or embryonal rhabdomyosarcoma-derived myoblasts. \"'), ('9880', 'SYT_SSX1', '', 'SYT', 'SSX1', '9788446', '2', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'The resulting SYT-SSX1/SSX2 proteins are activators of transcription. '), ('9881', 'FUS_CHOP ', '', 'FUS', 'CHOP ', '8058726', '2', 'liposarcoma', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'In the case of the liposarcoma, transactivation by the FUS-CHOP protein occurs because the FUS transcriptional activation domain is added to the DNA-binding CHOP protein normally lacking such activity.     ///    \"J, joining) and FUS-CHOP (a liposarcoma tumor-specific fusion protein that is produced as a result of a chromosomal translocation) can function as transcription activators of specific responsive reporter genes. \"    ///    Transcriptional activation by TAL1 and FUS-CHOP proteins expressed in acute malignancies as a result of chromosomal abnormalities.. '), ('9882', 'PAX3_FOXO1', '', 'PAX3', 'FOXO1', '24107448', '2', 'rhabdomyosarcoma;sarcoma\r\r', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', 'KB', 'Seq', 'In this study, we screened small molecule chemical libraries for inhibitors of PAX3-FOXO1 transcriptional activity using a cell-based readout system.    ///    \"In this study, we screened small molecule chemical libraries for inhibitors of PAX3-FOXO1 transcriptional activity using a cell-based readout system. \"    ///    \"The hallmark of the majority of alveolar rhabdomyosarcoma is a chromosomal translocation that generates the PAX3-FOXO1 fusion protein, which is an oncogenic transcription factor responsible for the development of the malignant phenotype of this tumor. \"    ///    \"Alveolar rhabdomyosarcoma cells are dependent on the oncogenic activity of PAX3-FOXO1, and its expression status in alveolar rhabdomyosarcoma tumors correlates with worst patient outcome, suggesting that blocking this activity of PAX3-FOXO1 may be an attractive therapeutic strategy against this fusion-positive disease. \"    ///    These data reveal that thapsigargin-induced activation of AKT is an effective mechanism to inhibit PAX3-FOXO1 and a potential agent for targeted therapy against alveolar rhabdomyosarcoma..     ///    We identified the Sarco/endoplasmic reticulum Ca(2+)-ATPases (SERCA) inhibitor thapsigargin as an effective inhibitor of PAX3-FOXO1.     ///    Small molecule inhibition of PAX3-FOXO1 through AKT activation suppresses malignant phenotypes of alveolar rhabdomyosarcoma..     ///    \"Furthermore, thapsigargin inhibited the binding of PAX3-FOXO1 to target genes and subsequently promoted its proteasomal degradation. \"    ///    Subsequent experiments in alveolar rhabdomyosarcoma cells showed that activation of AKT by thapsigargin inhibited PAX3-FOXO1 activity via phosphorylation. '), ('9883', 'EWS_ERG', '', 'EWS', 'ERG', '17690209', '2', '', '', '', '', '', '', '', '', '', 'EFTs show fusions of EWS with a gene of the ETS family of transcription factors, either EWS-FLI1 (90 to 95%) or EWS-ERG (5 to 10%). '), ('9884', 'RARA_PML', 't(15;17)(q22;q21) / t(15;17)  / ', 'RARA', 'PML', '7935403', '2', 'acute promyelocytic leukemia;leukemia\r\r', '', '', 'Oncogene', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'The breakpoint site encodes fusion protein PML-RAR alpha, which is able to form a heterodimer with PML. '), ('9885', 'PAX3_FOXO1', '', 'PAX3', 'FOXO1', '17986608', '2', 'rhabdomyosarcoma;sarcoma\r\r', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', 'KB', 'Seq', 'This defect is caused by reduced levels of the EGR1 transcriptional activator resulting from a direct, destabilizing interaction with PAX3-FOXO1.     ///    \"To understand how PAX3-FOXO1 contributes to tumor development, we isolated and characterized muscle cells from transgenic mice expressing PAX3-FOXO1 under control of the PAX3 promoter. \"    ///    PAX3-FOXO1 controls expression of the p57Kip2 cell-cycle regulator through degradation of EGR1..     ///    \"The chimeric protein PAX3-FOXO1, resulting from a translocation between chromosomes 2 and 13, is the most common genetic aberration in the alveolar subtype of the human skeletal muscle tumor, rhabdomyosarcoma.\"    ///    \" The chimeric protein PAX3-FOXO1, resulting from a translocation between chromosomes 2 and 13, is the most common genetic aberration in the alveolar subtype of the human skeletal muscle tumor, rhabdomyosarcoma. \"'), ('9886', 'PDGFB_COL1A1', '', 'PDGFB', 'COL1A1', '16126884', '2', 'dermatofibrosarcoma protuberans;sarcoma\r\r', '', '', 'Oncogene', '', '', '', 'KB', '', 'Reverse transcription polymerase chain reaction and sequence analysis showed the presence of an identical COL1A1-PDGFB fusion transcript in ordinary DFSP (plaque-like area), FS, and myxoid areas of DFSP. '), ('9887', 'PPARG_PAX8', '', 'PPARG', 'PAX8', '16179407', '2', 'thyroid carcinoma\r\r', '', '', '', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'In gel shift analyses, PAX8-PPARgamma bound a PPARgamma-response element suggesting that its transcriptional function is mediated via direct DNA contact.     ///    This study investigated the transcriptional mechanisms by which PAX8-PPARgamma regulates follicular thyroid cells.     ///    PAX8-peroxisome proliferator-activated receptor gamma (PPARgamma) disrupts normal PAX8 or PPARgamma transcriptional function and stimulates follicular thyroid cell growth..     ///    \"In HeLa cells, rat follicular thyroid (FRTL-5) cells, or immortalized human thyroid cells, PAX8-PPARgamma stimulated transcription from PAX8-responsive thyroperoxidase and sodium-iodide symporter promoters in a manner at least comparable with wild-type PAX8. \"    ///    \"Therefore, PAX8-PPARgamma disrupts normal transcriptional regulation by stimulating some genes and inhibiting others, the net effect of which may mediate follicular thyroid cell growth and loss of differentiation that ultimately leads to carcinogenesis.. \"    ///    \"Unexpectedly, PAX8-PPARgamma transcriptional function on a PPARgamma-responsive promoter was cell-type dependent. \"    ///    \"In contrast, PAX8-PPARgamma failed to stimulate transcription from the thyroglobulin promoter and blocked the synergistic stimulation of this promoter by wild-type PAX8 and thyroid transcription factor-1. \"    ///    \"In this model, PAX8-PPARgamma expression was associated with enhanced growth as assessed by soft agar assays and thymidine uptake. \"    ///    \"in HeLa cells, PAX8-PPARgamma dominantly inhibited expression of the PPARgamma-responsive promoter, whereas in FRTL-5 and immortalized human thyroid cells PAX8-PPARgamma stimulated this promoter. \"    ///    A biological model of PAX8-PPARgamma function in follicular thyroid cells was generated via constitutive expression of the fusion protein in FRTL-5 cells. '), ('9888', 'STAT6_NAB2', '', 'STAT6', 'NAB2', '23313954', '2', 'solitary fibrous tumor\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', '', 'Analysis in 53 tumors confirmed the presence of 7 variants of this fusion transcript in 29 tumors (55%), representing a lower bound for fusion frequency at this locus and suggesting that the NAB2-STAT6 fusion is a distinct molecular feature of SFTs..     ///    Whole-exome sequencing identifies a recurrent NAB2-STAT6 fusion in solitary fibrous tumors..     ///    \"Here, we describe the identification of a NAB2-STAT6 fusion from whole-exome sequencing of 17 SFTs. \"'), ('9889', 'TEC_EWS', '', 'TEC', 'EWS', '12049818', '2', 'chondrosarcoma;sarcoma\r\r', '', 'Kinase', '', '', '', '', '', '', 'These results suggest that EWS/TEC interacts at least in part with the same transcriptional coactivators as the native TEC receptor, and that these coactivators may be involved in the tumoral process leading to human chondrosarcoma tumors..     ///    \"Point mutation analyses indicate that within the AF2 domain, amino acid residues I939, D940 and F943 all play a crucial role in the activity of EWS/TEC. \"    ///     The EWS/TEC fusion protein encoded by the t(9:22) chromosomal translocation in human extraskeletal myxoid chondrosarcoma tumors is thought to participate in the tumoral process at least in part by deregulating the expression of specific target genes involved in the control of cell proliferation.     ///    The AF2 domain of the orphan nuclear receptor TEC is essential for the transcriptional activity of the oncogenic fusion protein EWS/TEC..     ///    In this work we show that the activation function-2 (AF2) domain of TEC is essential for the transcriptional activity of the EWS/TEC fusion protein. '), ('9890', 'RARA_PML', 't(15;17)  / ', 'RARA', 'PML', '9031108', '2', 'acute promyelocytic leukemia;leukemia\r\r', '', '', 'Oncogene', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'The fusion protein PML-RAR alpha encoded from the breakpoint can form a heterodimer and acts as a dominant negative inhibitor against the normal function of PML. '), ('9891', 'PLAG1_CHCHD7', '', 'PLAG1', 'CHCHD7', '21394649', '1', 'pleomorphic adenoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'RT-PCR analyses identified the CTNNB1-PLAG1, LIFR-PLAG1, CHCHD7-PLAG1, and HMGA2-WIF1 fusion transcripts in eight, two, one, and one case, respectively. '), ('9892', 'PLAG1_CTNNB1', '', 'PLAG1', 'CTNNB1', '21394649', '1', 'pleomorphic adenoma\r\r', 'PCR;RT-PCR', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', '', 'RT-PCR analyses identified the CTNNB1-PLAG1, LIFR-PLAG1, CHCHD7-PLAG1, and HMGA2-WIF1 fusion transcripts in eight, two, one, and one case, respectively. '), ('9893', 'PLAG1_LIFR', '', 'PLAG1', 'LIFR', '21394649', '1', 'pleomorphic adenoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'RT-PCR analyses identified the CTNNB1-PLAG1, LIFR-PLAG1, CHCHD7-PLAG1, and HMGA2-WIF1 fusion transcripts in eight, two, one, and one case, respectively.     ///    \"RT-PCR analyses identified the CTNNB1-PLAG1, LIFR-PLAG1, CHCHD7-PLAG1, and HMGA2-WIF1 fusion transcripts in eight, two, one, and one case, respectively.\"'), ('9894', 'RFG5_RET', '', 'RFG5', 'RET', '9443391', '1', 'thyroid carcinoma\r\r', 'PCR', 'Kinase', 'Oncogene', '', '', '', '', '', 'In addition to the RFG5/RET, we also detected the reciprocal RET/RFG5 transcript in both tumor samples, suggesting that the rearrangement is based on a balanced reciprocal translocation.     ///    \"Ret immunohistochemistry indicates that the fusion protein is expressed in all cells of PTC5 tumors, suggesting that RFG5/RET rearrangement is an early event in thyroid carcinogenesis.. \"'), ('9895', 'TCEA1_PLAG1', '', 'TCEA1', 'PLAG1', '21394649', '1', 'pleomorphic adenoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', 'KB', '', 'The TCEA1-PLAG1, HMGA2-FHIT, and HMGA2-NFIB fusion transcripts were not detected. '), ('9896', 'EWS_ERG', 't(11;22)(q24;q12) / t(21;22)(q22;q12) / ', 'EWS', 'ERG', '7591257', '1', 'neuroectodermal tumor;ewing sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'We detected 2 types of EWS-ERG chimeric mRNA in 2 ES cell lines and 1 PNET tumor sample in addition to 4 types of EWS-FLI-1 chimeric mRNA in 11 ESs (4 cell lines and 7 tumor samples) and 4 PNETs (2 cell lines and 2 tumor samples).     ///    EWS-FLI-1 and EWS-ERG chimeric mRNAs in Ewing\'s sarcoma and primitive neuroectodermal tumor.. '), ('9897', 'KIAA1549_BRAF', '', 'KIAA1549', 'BRAF', '24057326', '0', 'pilocytic astrocytoma;glioblastoma multiforme\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'BRAF-KIAA1549 fusion status was assessed in the PA subgroup.     ///    The rate of BRAF-KIAA1549 fusion was high in these PAs (5/7 tumors) including four extracerebellar examples.     ///    \"These results suggest that (a) BRAF-KIAA1549 fusion may be common in PAs with atypical clinicoradiologic and histologic features, including those at extracerebellar sites, (b) BRAF V600E mutation is uncommon in extracerebellar PAs, and (c) TP53 mutation analysis remains a valuable tool in identifying childhood gliomas that will likely behave in a malignant fashion.. \"    ///    \"These results suggest that (a) BRAF-KIAA1549 fusion may be common in PAs with atypical clinicoradiologic and histologic features, including those at extracerebellar sites, (b) BRAF V600E mutation is uncommon in extracerebellar PAs, and (c) TP53 mutation analysis remains a valuable tool in identifying childhood gliomas that will likely behave in a malignant fashion..\"'), ('9898', 'NAB2_STAT6', '', 'NAB2', 'STAT6', '24703527', '0', 'solitary fibrous tumor\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', '', 'Although the definite diagnosis is difficult in the settings of the unusual histology and the deficiency of NAB2-STAT6 fusion, it is possible that this STAT6-positive intraorbital papillary tumor is a very rare variant of solitary fibrous tumor.    ///    \"Although the definite diagnosis is difficult in the settings of the unusual histology and the deficiency of NAB2-STAT6 fusion, it is possible that this STAT6-positive intraorbital papillary tumor is a very rare variant of solitary fibrous tumor. \"'), ('9899', 'KIF5B_RET', '', 'KIF5B', 'RET', '22928112', '0', 'non small cell lung cancer;non small cell lung cancer;small cell lung c\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'It is now clear that heterogeneous cell signaling pathways are disrupted to promote NSCLC, including mutations in critical growth regulatory proteins (K-Ras, EGFR, B-RAF, MEK-1, HER2, MET, EML-4-ALK, KIF5B-RET, and NKX2.1) and inactivation of growth inhibitory pathways (TP53, PTEN, p16, and LKB-1).    ///    \"It is now clear that heterogeneous cell signaling pathways are disrupted to promote NSCLC, including mutations in critical growth regulatory proteins (K-Ras, EGFR, B-RAF, MEK-1, HER2, MET, EML-4-ALK, KIF5B-RET, and NKX2.1) and inactivation of growth inhibitory pathways (TP53, PTEN, p16, and LKB-1). \"'), ('9900', 'EML4_ALK', '', 'EML4', 'ALK', '20075203', '0', '', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'EML4-ALK fusion in lung.    ///    EML4-ALK fusion in lung.. '), ('9901', 'KIF5B_RET', '', 'KIF5B', 'RET', '23378251', '0', 'neuroectodermal tumor;squamous cell carcinoma', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The objective of the current study was to determine the prevalence and clinicopathologic characteristics of KIF5B-RET fusions (fusions of the RET and kinesin family member 5B [KIF5B] genes) in Chinese patients with NSCLC.    ///    \"There was no statistically significant difference in age, sex, smoking status, pathologic stage, or histologic type between patients with and without KIF5B-RET fusions.\"    ///    All patients who were positive for a KIF5B-RET fusion were never-smokers.    ///    \"KIF5B-RET fusions were quite rare, with a prevalence of approximately 1.5% in Chinese patients with NSCLC, and they were a little more common in patients with adenocarcinoma than in those with squamous carcinoma (1.73% vs 0.84%).\"    ///    The relations between KIF5B-RET fusions and clinicopathologic characteristics were analyzed.     ///    KIF5B-RET fusions in Chinese patients with non-small cell lung cancer..     ///    \"In total, 6 patients (1.5%) were identified who harbored KIF5B-RET fusions. \"    ///    \"Patients without KIF5B-RET fusions had a better prognosis than those with KIF5B-RET fusions (median survival, 52.6 months vs 21.0 months. \"    ///    The authors screened for KIF5B-RET fusions in 392 patients with NSCLC using multiplex real-time polymerase chain reaction assay and validated all positive samples using direct sequencing.     ///    \"There was no statistically significant difference in age, sex, smoking status, pathologic stage, or histologic type between patients with and without KIF5B-RET fusions. \"    ///    \"KIF5B-RET fusions were quite rare, with a prevalence of approximately 1.5% in Chinese patients with NSCLC, and they were a little more common in patients with adenocarcinoma than in those with squamous carcinoma (1.73% vs 0.84%). \"    ///    \"In addition, KIF5B-RET fusions also existed in patients with low-grade malignant neuroendocrine tumors.. \"'), ('9902', 'EML4_ALK', '', 'EML4', 'ALK', '26517679', '0', 'non small cell lung cancer;non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Here, we report that stem-like properties stem from ALK activity in EML4-ALK+ NSCLC cells.     ///    \"Although the inhibitor crizotinib, as it blocks the kinase activity of the resulting EML4-ALK fusion protein, displays remarkable initial responses, a fraction of NSCLC cases eventually become resistant to crizotinib by acquiring mutations in the ALK domain or activating bypass pathways via EGFR, KIT, or KRAS.\"    ///    \"Although the inhibitor crizotinib, as it blocks the kinase activity of the resulting EML4-ALK fusion protein, displays remarkable initial responses, a fraction of NSCLC cases eventually become resistant to crizotinib by acquiring mutations in the ALK domain or activating bypass pathways via EGFR, KIT, or KRAS. \"'), ('9903', 'KIAA1549_BRAF', '', 'KIAA1549', 'BRAF', '24806303', '0', 'pilocytic astrocytoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'They are considered to be the most frequent mechanism of mitogen-activated protein kinase activation, alternative to KIAA1549-BRAF fusion and BRAF mutations.    ///    \"They are considered to be the most frequent mechanism of mitogen-activated protein kinase activation, alternative to KIAA1549-BRAF fusion and BRAF mutations. \"    ///    \"Despite their histologic similarity with pilocytic astrocytomas (PAs), RGNTs do not harbor KIAA1549-BRAF fusions or BRAF mutations, which represent the most common genetic alteration in PAs. \"'), ('9904', 'RET_KIF5B', '', 'RET', 'KIF5B', '24481316', '0', 'squamous cell carcinoma;lung cancer;adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'Of the 76 AdSqLCs, 43 (56.6%) harbored known mutant kinases, including 24 (31.6%) with EGFR mutations, eight (10.5%) with KRAS mutations, two (2.6%) with AKT1 (2.6%) mutations, one (1.3%) with ERBB2 insertion mutation, one (1.3%) with PIK3CA mutation, four (5.3%) with ALK fusions, and three (4%) with KIF5B-RET fusions. '), ('9905', 'CD74_ROS1', '', 'CD74', 'ROS1', '25733882', '0', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'In vivo, PF-06463922 showed marked antitumor activity in tumor models expressing FIG-ROS1, CD74-ROS1, and the CD74-ROS1(G2032R) mutation.    ///    \"In vivo, PF-06463922 showed marked antitumor activity in tumor models expressing FIG-ROS1, CD74-ROS1, and the CD74-ROS1(G2032R) mutation. \"'), ('9906', 'KIAA1549_BRAF', '', 'KIAA1549', 'BRAF', '25667294', '0', '', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Alterations in chromatin-modifying genes and telomere-maintenance pathways were commonly observed, whereas no sHGG harbored the BRAF-KIAA1549 fusion.    ///    \"Alterations in chromatin-modifying genes and telomere-maintenance pathways were commonly observed, whereas no sHGG harbored the BRAF-KIAA1549 fusion. \"'), ('9907', 'KIAA1549_BRAF', '', 'KIAA1549', 'BRAF', '24767714', '0', 'fibrillary astrocytoma;medulloblastoma', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Nineteen of 56 low grade gliomas (LGGs) demonstrated a duplication in 7q34, which resulted in a KIAA1549-BRAF fusion. '), ('9908', 'BCR_ABL1', '', 'BCR', 'ABL1', '25913326', '0', 'chronic myeloid leukemia;myeloid leukemia;leukemia\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'A thirty-five nucleotides BCR-ABL1 insertion mutation of controversial significance confers resistance to imatinib in a patient with chronic myeloid leukemia (CML)..     ///    \"Although deletion or insertion of nucleotides in BCR-ABL1 has rarely been described, we identified a CML patient with an already described 35 nucleotides insertion (BCR-ABL1(35INS)) of controversial significance, that confers resistance to imatinib but sensitivity to dasatinib.. \"'), ('9909', 'KIAA1549_BRAF', '', 'KIAA1549', 'BRAF', '23612919', '0', 'astrocytoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The majority involved the KIAA1549-BRAF exon 16-exon 9 variant. '), ('9910', 'SYT_SSX2', '', 'SYT', 'SSX2', '12173050', '0', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'and (2) that the SYT-SSX1 fusion type has a stronger influence on these mechanisms than SYT-SSX2.     ///    \"In this study we made use of the SYT-SSX1 vs SYT-SSX2 concept to investigate whether major, tumour relevant, and growth regulatory proteins (e.g. \"    ///    \" A recent large multi-centre study convincingly confirmed previous observations that the SYT-SSX1 fusion type, compared to SYT-SSX2, of synovial sarcoma is associated with a worse clinical outcome. \"'), ('9911', 'BCR_ABL1', '', 'BCR', 'ABL1', '20447687', '0', 'chronic myeloid leukemia;myeloid leukemia;leukemia\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'A T315I mutation in e19a2 BCR/ABL1 chronic myeloid leukemia responding to dasatinib.. '), ('9912', 'EML4_ALK', '', 'EML4', 'ALK', '24618813', '0', '', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Abrogation of EML4-ALK in H2228 cells profoundly reduced signaling capacity of the rapamycin-sensitive mTOR pathway leading to G 1 cell cycle arrest and mitochondrial hyperpolarization, a metabolic perturbation linked to mTOR inhibition.    ///    \"Abrogation of EML4-ALK in H2228 cells profoundly reduced signaling capacity of the rapamycin-sensitive mTOR pathway leading to G 1 cell cycle arrest and mitochondrial hyperpolarization, a metabolic perturbation linked to mTOR inhibition. \"    ///    \"CM-118 potently abrogated hepatocyte growth factor (HGF)-induced c-Met phosphorylation and cell migration, phosphorylation of ALK, EML4-ALK, and ALK resistance mutants in transfected cells. \"'), ('9913', 'EML4_ALK', '', 'EML4', 'ALK', '24952482', '0', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'These results suggest that Hsp90 inhibitors may overcome ligand-triggered resistance to new generation ALK inhibitors and may result in more successful treatment of NSCLC patients with EML4-ALK..    ///    These results suggest that Hsp90 inhibitors may overcome ligand-triggered resistance to new generation ALK inhibitors and may result in more successful treatment of NSCLC patients with EML4-ALK..     ///    Receptor ligand-triggered resistance to alectinib and its circumvention by Hsp90 inhibition in EML4-ALK lung cancer cells..     ///    \"Additionally, the heat shock protein 90 (Hsp90) inhibitor suppressed protein expression of ALK, MET, EGFR, and AKT, and thereby induced apoptosis in EML4-ALK NSCLC cells, even in the presence of EGFR ligands or HGF. \"'), ('9914', 'HIP1_ALK', '', 'HIP1', 'ALK', '25393796', '0', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', '', 'However, the response of patients with NSCLC harboring HIP1-ALK to ALK inhibitors and potential resistance mechanisms to such remain unknown.     ///    \"To date, two variants of HIP1-ALK (H21. \"    ///    Identification of a novel HIP1-ALK fusion variant in Non-Small-Cell Lung Cancer (NSCLC) and discovery of ALK I1171 (I1171N/S) mutations in two ALK-rearranged NSCLC patients with resistance to Alectinib..     ///    \"Here, we report a patient with NSCLC harboring a novel HIP1-ALK fusion variant (H30. \"    ///    \"Here, we report a patient with NSCLC harboring a novel HIP1-ALK fusion variant (H30; A20).\"'), ('9915', 'EWSR1_CREB1', '', 'EWSR1', 'CREB1', '23953591', '0', 'clear cell sarcoma;sarcoma\r\r', '', '', '', '', '', 'Transcription_Factor', 'KB', '', 'We examined EWSR1-ATF1 and EWSR1-CREB1 fusions in a single case of clear cell sarcoma with lung metastasis in a 36-year-old Japanese man.    ///    Clear cell sarcoma is a unique tumor which has EWSR1-ATF1 or EWSR1-CREB1 fusion.    ///     Clear cell sarcoma is a unique tumor which has EWSR1-ATF1 or EWSR1-CREB1 fusion. '), ('9916', 'EML4_ALK', '', 'EML4', 'ALK', '26168728', '0', '', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Development of potent ALK inhibitor and its molecular inhibitory mechanism against NSCLC harboring EML4-ALK proteins.    ///    \"Cell based assays demonstrate our compounds downregulate the cellular signaling, such as Akt and Erk, by suppressing ALK activity to inhibit the proliferation of the cells harboring EML4-ALK. \"    ///    Development of potent ALK inhibitor and its molecular inhibitory mechanism against NSCLC harboring EML4-ALK proteins..     ///    \" Here, we show the newly synthesized and potent ALK inhibitor having similar scaffold to KRCA-0008, which was reported previously, and its molecular mechanism against cancer cells harboring EML4-ALK fusion protein. \"'), ('9917', 'TMPRSS2_ERG', '', 'TMPRSS2', 'ERG', '25933120', '0', 'prostate cancer\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'Microarray analysis further confirmed ERG inhibition by both siRNAs TMPRSS2-ERG and revealed one common down-regulated gene, ADRA2A, involved in cell proliferation and migration.    ///    Two of the five siRNAs tested were found to efficiently inhibit mRNA of both TMPRSS2-ERG variants and to decrease ERG protein expression.    ///    \"In conclusion, this study offers a new prospect of treatment for prostate cancer based on siRNA-squalene nanoparticles targeting TMPRSS2-ERG junction oncogene. \"    ///    \"Microarray analysis further confirmed ERG inhibition by both siRNAs TMPRSS2-ERG and revealed one common down-regulated gene, ADRA2A, involved in cell proliferation and migration. \"    ///     TMPRSS2-ERG junction oncogene is present in more than 50% of patients with prostate cancer and its expression is frequently associated with poor prognosis.     ///    \"To propose a concrete therapeutic approach, siRNA TMPRSS2-ERG IV was conjugated to squalene, which can self-organize as nanoparticles in water. \"    ///    Antineoplastic Effects of siRNA against TMPRSS2-ERG Junction Oncogene in Prostate Cancer..     ///    Our aim is to achieve gene knockdown by siRNA TMPRSS2-ERG and then to assess the biological consequences of this inhibition. ');
INSERT INTO `ChimerPub_dump` VALUES ('9918', 'MYB_NFIB', '', 'MYB', 'NFIB', '23825564', '0', 'acinic cell carcinoma', '', '', '', '', '', '', 'KB', 'Seq', 'The results were also collected with the MYB-NFIB fusion status and the clinicopathologic features.    ///    No significant differences in miRNA expression were found between the MYB-NFIB fusion positive and -negative ACCs. '), ('9919', 'EML4_ALK', '', 'EML4', 'ALK', '22553343', '0', 'lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Paracrine receptor activation by microenvironment triggers bypass survival signals and ALK inhibitor resistance in EML4-ALK lung cancer cells.    ///    \"We tested the effects of ligands produced by endothelial cells and fibroblasts, and the cells themselves, on the susceptibility of EML4-ALK lung cancer cell lines to crizotinib and TAE684, a selective ALK inhibitor active against cells with ALK amplification and gatekeeper mutations, both in vitro and in vivo.\"    ///    We determined whether microenvironmental factors trigger ALK inhibitor resistance in EML4-ALK lung cancer cells.     ///    EML4-ALK lung cancer cells were highly sensitive to ALK inhibitors.     ///    \"Paracrine receptor activation by ligands from the microenvironment may trigger resistance to ALK inhibitors in EML4-ALK lung cancer cells, suggesting that receptor ligands from microenvironment may be additional targets during treatment with ALK inhibitors.. \"    ///    \"Although crizotinib, a dual tyrosine kinase inhibitor (TKI) of ALK and Met, shows dramatic effect against EML4-ALK lung cancer cells, these cells can acquire resistance to crizotinib by several mechanisms, including ALK amplification and gatekeeper mutation. \"    ///    Paracrine receptor activation by microenvironment triggers bypass survival signals and ALK inhibitor resistance in EML4-ALK lung cancer cells..     ///    \"Endothelial cells and fibroblasts, which produce the EGFR ligands and HGF, respectively, decreased the sensitivity of EML4-ALK lung cancer cells to crizotinib and TAE684, respectively. \"    ///    \"We tested the effects of ligands produced by endothelial cells and fibroblasts, and the cells themselves, on the susceptibility of EML4-ALK lung cancer cell lines to crizotinib and TAE684, a selective ALK inhibitor active against cells with ALK amplification and gatekeeper mutations, both in vitro and in vivo. \"'), ('9920', 'NRG1_CD74', '', 'NRG1', 'CD74', '24727320', '0', 'adenocarcinoma\r\r', '', '', '', '', '', '', '', '', 'We identified oncogenic fusions that occurred mutually exclusively with KRAS mutations: CD74-NRG1, SLC3A2-NRG1, EZR-ERBB4, TRIM24-BRAF, and KIAA1468-RET.     ///    \"The CD74-NRG1 fusion activated HER2:HER3 signaling, whereas the EZR-ERBB4 and TRIM24-BRAF fusions constitutively activated the ERBB4 and BRAF kinases, respectively. \"'), ('9921', 'ASPSCR1_TFE3', 't(X;17)(p11.2;q25) / / ', 'ASPSCR1', 'TFE3', '20002771', '0', 'alveolar soft part sarcoma', '', '', 'Oncogene', '', '', '', 'KB', 'Seq', 'Activated c-Met and the phosphorylation of its downstream effectors validate an intact signalling cascade probably induced by the ASPSCR1-TFE3 chimeric transcription factor.    ///    Activated c-Met and the phosphorylation of its downstream effectors validate an intact signalling cascade probably induced by the ASPSCR1-TFE3 chimeric transcription factor. '), ('9922', 'BCR_ABL1', '', 'BCR', 'ABL1', '24752059', '0', 'chronic myeloid leukemia;myeloid leukemia;leukemia\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Molecular Response of e19a2 BCR-ABL1 Chronic Myeloid Leukemia With Double Philadelphia Chromosome to Dasatinib.. '), ('9923', 'TPM4_ALK', '', 'TPM4', 'ALK', '17694547', '0', 'non Hodgkin lymphoma;breast cancer;anaplastic large cell lymphoma;neuroblastoma;sarcoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'In addition, two recent reports have suggested that the ALK fusion, TPM4-ALK, may be involved in the genesis of a subset of esophageal squamous cell carcinomas.    ///    \"In addition, two recent reports have suggested that the ALK fusion, TPM4-ALK, may be involved in the genesis of a subset of esophageal squamous cell carcinomas. \"'), ('9924', 'BCR_JAK2', '', 'BCR', 'JAK2', '25664618', '0', '', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'In this study, we demonstrated that in vivo expression of BCR-JAK2 in mice induces neoplasia, with fatal consequences.'), ('9925', 'EML4_ALK', '', 'EML4', 'ALK', '23723294', '0', 'non small cell lung cancer', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Genes evaluated were TP53, EGFR, KRAS, LKB1, EML4-ALK, PTEN, BRAF, PIK3CA, and ErbB2.    ///    \"Genes evaluated were TP53, EGFR, KRAS, LKB1, EML4-ALK, PTEN, BRAF, PIK3CA, and ErbB2. \"'), ('9926', 'NCOA4_RET', '', 'NCOA4', 'RET', '23856031', '0', 'lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'In cellular assays, lenvatinib inhibited auto-phosphorylation of KIF5B-RET, CCDC6-RET, and NcoA4-RET.    ///    \"In cellular assays, lenvatinib inhibited auto-phosphorylation of KIF5B-RET, CCDC6-RET, and NcoA4-RET. \"'), ('9927', 'PAX3_FOXO1', '', 'PAX3', 'FOXO1', '24797362', '0', 'rhabdomyosarcoma;sarcoma\r\r', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', 'KB', 'Seq', 'Moreover, Notch3 depletion reduces PAX3-FOXO1 alveolar RMS tumor growth in vivo.    ///    \"Moreover, Notch3 depletion reduces PAX3-FOXO1 alveolar RMS tumor growth in vivo. \"    ///    \"The majority of alveolar RMS expresses PAX3-FOXO1 fusion oncoprotein, associated with the worst prognosis. \"'), ('9928', 'MLL_ELL', '', 'MLL', 'ELL', '25758097', '0', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'Intriguingly, clonally expanded non-leukemic cells expressing MLL-ELL during consolidation therapy were found to be eradicated after allo-HSCT during the monitoring of minimal residual disease in one patient.     ///    \"In conclusion, allo-HSCT soon after CR1 represents a promising therapeutic option for adult AML patients with MLL-ELL, although the outcome of allo-HSCT for patients beyond CR1 was dismal.. \"    ///     Acute myeloid leukemia (AML) with mixed lineage leukemia-eleven-nineteen lysine-rich leukemia (MLL-ELL) is a rare subtype of MLL-rearranged AML. '), ('9929', 'WT1_EWS', 't(11;22)(p13;q12) / ', 'WT1', 'EWS', '11480729', '0', 'desmoplastic small round cell tumor \r\r', '', '', '', '', '', '', '', '', 'Molecular analysis was performed on FNA, revealing the EWS/ WT1 chimeric transcript and thus confirming the cytologic diagnosis. '), ('9930', 'TFE3_ASPL', '', 'TFE3', 'ASPL', '18594808', '0', 'alveolar soft part sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'This is the first case of alveolar soft part sarcoma in bone documenting the ASPL-TFE3 gene product.     ///    Primary alveolar soft part sarcoma of fibula demonstrating ASPL-TFE3 fusion: a case report and review of the literature.. '), ('9931', 'TPM3_ALK', '', 'TPM3', 'ALK', '20870660', '0', '', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Malignant high-grade histological transformation of inflammatory myofibroblastic tumour associated with amplification of TPM3-ALK.    ///    Malignant high-grade histological transformation of inflammatory myofibroblastic tumour associated with amplification of TPM3-ALK.. '), ('9932', 'MLL_EPS15', '', 'MLL', 'EPS15', '19665789', '0', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'A novel MLL-AF1p/Eps15 fusion variant in therapy-related acute lymphoblastic leukemia, lacking the EH-domains.. '), ('9933', 'RET_CCDC6', '', 'RET', 'CCDC6', '22327623', '0', 'lung cancer;adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'In addition, we discovered previously unidentified kinase fusions that may be promising for molecular-targeted therapy, kinesin family member 5B (KIF5B)-ret proto-oncogene (RET) and coiled-coil domain containing 6 (CCDC6)-RET, in 14 adenocarcinomas. '), ('9934', 'PDGFB_COL1A1', '', 'PDGFB', 'COL1A1', '12660034', '0', 'dermatofibrosarcoma protuberans;sarcoma\r\r', '', '', 'Oncogene', '', '', '', 'KB', '', 'To confirm the diagnosis, molecular studies were performed on fixed tumor and revealed the presence of the fusion product of the COL1A1-PDGFB genes characteristic of DFSP.. '), ('9935', 'EML4_ALK', '', 'EML4', 'ALK', '20979473', '0', 'small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', ' The EML4 (echinoderm microtubule-associated protein-like 4)-ALK (anaplastic lymphoma kinase) fusion-type tyrosine kinase is an oncoprotein found in 4 to 5% of non-small-cell lung cancers, and clinical trials of specific inhibitors of ALK for the treatment of such tumors are currently under way.     ///    \"Here, we report the discovery of two secondary mutations within the kinase domain of EML4-ALK in tumor cells isolated from a patient during the relapse phase of treatment with an ALK inhibitor. \"    ///    EML4-ALK mutations in lung cancer that confer resistance to ALK inhibitors.. '), ('9936', 'TRIM33_RET', '', 'TRIM33', 'RET', '23533264', '0', 'lung cancer;non small cell lung cancer', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Confirmed partial responses were observed in 2 patients, including one harboring a novel TRIM33-RET fusion.    ///    \"Confirmed partial responses were observed in 2 patients, including one harboring a novel TRIM33-RET fusion. \"'), ('9937', 'EWSR1_ATF1', '', 'EWSR1', 'ATF1', '23953591', '0', 'clear cell sarcoma;sarcoma\r\r', '', '', '', '', '', 'Transcription_Factor', 'KB', 'Seq', 'Clear cell sarcoma is a unique tumor which has EWSR1-ATF1 or EWSR1-CREB1 fusion.    ///     Clear cell sarcoma is a unique tumor which has EWSR1-ATF1 or EWSR1-CREB1 fusion.     ///    \"In our case, increased splicing activity in the EWSR1-ATF1 fusion might be acquired at the metastatic site. \"    ///    We examined EWSR1-ATF1 and EWSR1-CREB1 fusions in a single case of clear cell sarcoma with lung metastasis in a 36-year-old Japanese man.     ///    \"As a result, we found only type 1 EWSR1-ATF1 fusion in the primary site, but 4 types of EWS-ATF1 fusion (type 1, 2, 5, 6) were detected in the metastatic site. \"    ///    Several patterns of EWSR1-ATF1 fusion are observed in clear cell sarcoma.     ///    A rare case of clear cell sarcoma with 4 types of EWSR1-ATF1 fusions detected not in primary site but in metastatic site.. '), ('9938', 'EML4_ALK', '', 'EML4', 'ALK', '22443113', '0', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The echinoderm microtubule-associated protein like-4-anaplastic lymphoma kinase (EML4-ALK) fusion oncogene represents one of the newest molecular targets in NSCLC, identifying a subset of NSCLC patients characterized by distinct clinicopathological features.    ///    \"The echinoderm microtubule-associated protein like-4-anaplastic lymphoma kinase (EML4-ALK) fusion oncogene represents one of the newest molecular targets in NSCLC, identifying a subset of NSCLC patients characterized by distinct clinicopathological features. \"'), ('9939', 'EML4_ALK', '', 'EML4', 'ALK', '26237499', '0', 'non small cell lung cancer;lung cancer;hepatocel\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Lung adenocarcinoma includes recurrent activating oncogenic mutations (EGFR, EML4-ALK, ROS1) that have been associated with response to EGFR and ALK inhibitors.    ///    \" Lung adenocarcinoma includes recurrent activating oncogenic mutations (EGFR, EML4-ALK, ROS1) that have been associated with response to EGFR and ALK inhibitors. \"'), ('9940', 'EML4_ALK', '', 'EML4', 'ALK', '23443800', '0', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'ALK inhibitor PF02341066 (crizotinib) increases sensitivity to radiation in non-small cell lung cancer expressing EML4-ALK.    ///    \"Our findings indicate that PF02341066 acts as a radiation sensitizer in cells harboring the EML4-ALK fusion, providing a rationale for a clinical trial combining ALK inhibitor with radiation in the NSCLCs expressing ALK..\"    ///    ALK inhibitor PF02341066 (crizotinib) increases sensitivity to radiation in non-small cell lung cancer expressing EML4-ALK..     ///    \"Our findings indicate that PF02341066 acts as a radiation sensitizer in cells harboring the EML4-ALK fusion, providing a rationale for a clinical trial combining ALK inhibitor with radiation in the NSCLCs expressing ALK.. \"    ///    \"To further elucidate the role of PF02341066 in tumor inhibition, we examined its effects alone and in combination with radiation on downstream signaling, apoptosis, and radiosensitivity in two NSCLC cell lines in vitro: H3122, which harbors the EML4-ALK fusion, and H460, which does not. \"'), ('9941', 'KIAA1549_BRAF', '', 'KIAA1549', 'BRAF', '22710963', '0', 'pilocytic astrocytoma', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'KIAA1549-BRAF fusion was detected in 4 PA, \"diffuse variant,\" 2 DA, and 2 low-grade astrocytomas, subtype indeterminate, indicating that these tumors were molecularly consistent with PA, the most common subtype of the series.     ///    These results suggest that KIAA1549-BRAF fusion status and IDH1/2 and BRAF V600E mutational analyses may assist in the histologic classification of this diagnostically challenging group of tumors and result in a more accurate and objective combined molecular and histologic classification.. '), ('9942', 'SYT_SSX1', '', 'SYT', 'SSX1', '12173050', '0', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Using Western blotting analysis on 74 fresh, fusion variant-typed, tumour samples from localized synovial sarcoma, we found a significant correlation between SYT-SSX1 and high expression of cyclin A (P=0.003) and D1 (P=0.025).     ///    \"Our data suggest that SYT-SSX may influence the cell cycle machinery, and that the more aggressive phenotype of the SYT-SSX1 variant is due to an accelerated tumour cell proliferation.. \"    ///    \"In this study we made use of the SYT-SSX1 vs SYT-SSX2 concept to investigate whether major, tumour relevant, and growth regulatory proteins (e.g. \"    ///    and (2) that the SYT-SSX1 fusion type has a stronger influence on these mechanisms than SYT-SSX2.     ///    \" A recent large multi-centre study convincingly confirmed previous observations that the SYT-SSX1 fusion type, compared to SYT-SSX2, of synovial sarcoma is associated with a worse clinical outcome. \"    ///    The SYT-SSX1 fusion type of synovial sarcoma is associated with increased expression of cyclin A and D1. '), ('9943', 'EWS_ETV1', '', 'EWS', 'ETV1', '9738976', '0', 'ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'EWS-FLI-1, EWS-ERG, EWS-ETV1 and EWS-FEV. '), ('9944', 'EML4_ALK', '', 'EML4', 'ALK', '25364516', '0', 'lung cancer;adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Nineteen EGFR mutations (52.8%), 3 KRAS mutations (8.3%), 2 EML4-ALK fusions (5.6%) and 1 KIF5b-RET fusion (2.8%) were identified in the younger group.    ///    \"Nineteen EGFR mutations (52.8%), 3 KRAS mutations (8.3%), 2 EML4-ALK fusions (5.6%) and 1 KIF5b-RET fusion (2.8%) were identified in the younger group. \"'), ('9945', 'EML4_ALK', '', 'EML4', 'ALK', '22007174', '0', '', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Some examples, including BCR-Abl, EML4-ALK, and the androgen receptor, contain mutations in the target itself, which hamper binding and inhibitory functions of therapeutic agents.    ///    \"Some examples, including BCR-Abl, EML4-ALK, and the androgen receptor, contain mutations in the target itself, which hamper binding and inhibitory functions of therapeutic agents. \"'), ('9946', 'FGFR3_TACC3', '', 'FGFR3', 'TACC3', '25950492', '0', 'breast cancer', '', 'Kinase', '', '', '', '', 'KB', 'Seq', 'Of 391 patients, 56 (14.3%) had aberrant FGF (N = 38, all amplifications) and/or FGFR (N = 22 including 5 mutations and one FGFR3-TACC3 fusion).'), ('9947', 'EML4_ALK', '', 'EML4', 'ALK', '20578368', '0', 'lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', '[Discovery of EML4-ALK, a new gene responsible for lung cancer, and the development of molecular targeted therapy].    ///    \"[Discovery of EML4-ALK, a new gene responsible for lung cancer, and the development of molecular targeted therapy].. \"'), ('9948', 'EML4_ALK', '', 'EML4', 'ALK', '23439505', '0', 'adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'In conclusion, NFKBIA expression was silenced in adenocarcinomas without EGFR/K-ras mutations or EML4-ALK fusion, suggesting that the silencing of NFKBIA may play an important role in the carcinogenesis of adenocarcinomas independent of EGFR/K-ras mutations or EML4-ALK fusion..     ///    \"EGFR and K-ras mutations and EML4-ALK fusion were detected in 61 (60.5%), 1 (1.0%), and 2 (2.0%) of the 101 samples, respectively, in a completely mutually exclusive manner. \"    ///    \"We examined NFKBIA expression, mutations in the EGFR and K-ras genes, and EML4-ALK fusion in 101 resected lung adenocarcinoma samples from never-smokers. \"'), ('9949', 'FAM131B_BRAF', '', 'FAM131B', 'BRAF', '24767714', '0', 'fibrillary astrocytoma;medulloblastoma', '', 'Kinase', 'Oncogene', '', '', '', 'KB', '', 'Chromosome band 7q34 deletions, which resulted in a FAM131B-BRAF fusion, were identified in one pilocytic astrocytoma (PA) and one dysembryoplastic neuroepithelial tumor (DNT). '), ('9950', 'TCF3_PBX1', '', 'TCF3', 'PBX1', '18024406', '0', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia\r\r', '', '', '', '', '', 'Transcription_Factor', 'KB', 'Seq', 'These data document that contemporary ALL-BFM treatment is highly effective in children with TCF3-PBX1 ALL.    ///    Patients with TCF3-PBX1 ALL treated on the ALL-BFM 86 trial had a poorer outcome than patients with TCF3-PBX1 ALL treated on later trials.     ///    \"Of 859 children with ALL who were treated in ALL-BFM trials in Austria, 31 (3.6%) had a TCF3-PBX1 ALL. \"    ///     Lessons from the analysis of children with TCF3-PBX1 ALL could help to identify treatment components essential for this leukemia subtype. '), ('9951', 'PAX7_FOXO1', '', 'PAX7', 'FOXO1', '25810375', '0', 'liposarcoma;rhabdomyosarcoma;neuroblastoma;sarcoma\r\r', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', 'KB', 'Seq', 'Rhabdomyosarcoma (RMS) is the most common pediatric soft tissue sarcoma and includes a PAX3- or PAX7-FOXO1 fusion-positive subtype.    ///     Rhabdomyosarcoma (RMS) is the most common pediatric soft tissue sarcoma and includes a PAX3- or PAX7-FOXO1 fusion-positive subtype. '), ('9952', 'FGFR3_ETV6', 't(4;12)(p16;p13) / ', 'FGFR3', 'ETV6', '11731410', '0', 'T cell lymphoma;lymphoma\r\r', '', 'Kinase', '', '', '', '', '', '', 'The ETV6-FGFR3 transcript showed a fusion of exon 5 of ETV6 to exon 10 of FGFR3, resulting in an open reading frame for a chimeric protein consisting of the HLH domain of ETV6 and the TK domains of FGFR3. '), ('9953', 'ETV6_NTRK3', '', 'ETV6', 'NTRK3', '17409427', '0', '', '', 'Kinase', '', '', '', '', 'KB', 'Seq', 'However, in Src-deficient cells, the ETV6-NTRK3 failed to activate the PI3K-Atk pathway, but not the Ras-Erk1/2 pathway.    ///    \"The ETV6-NTRK3 (EN) chimeric tyrosine kinase, a potent oncoprotein expressed in tumors derived from multiple cell lineages, functions as a constitutively active protein-tyrosine kinase.\"'), ('9954', 'CHCHD7_PLAG1', '', 'CHCHD7', 'PLAG1', '25931611', '0', '', '', '', '', '', '', '', 'KB', 'Seq', 'Of these 12 candidate gene regions, three contained known genes (i.e., NCAPG-LCORL, FBP2-PTCH1, and PLAG1-CHCHD7) related to bovine stature, and nine were not previously described in cattle (five in European and four in African cohorts).    ///    \"Of these 12 candidate gene regions, three contained known genes (i.e., NCAPG-LCORL, FBP2-PTCH1, and PLAG1-CHCHD7) related to bovine stature, and nine were not previously described in cattle (five in European and four in African cohorts). \"'), ('9955', 'PCM1_JAK2', '', 'PCM1', 'JAK2', '16007127', '0', 'myeloproliferative disorder;leukemia\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', '', 'A translocation generating the constitutively activated fusion protein PCM1-JAK2 has also been recently found in atypical chronic myelogenous leukemia and acute leukemia.    ///    A translocation generating the constitutively activated fusion protein PCM1-JAK2 has also been recently found in atypical chronic myelogenous leukemia and acute leukemia. '), ('9956', 'EML4_ALK', '', 'EML4', 'ALK', '23802852', '0', 'lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Targetable biomarkers other than EGFR and EML4-ALK were identified in 7 of the 40 Hispanic patients (18%) and 5 of the 43 non-Hispanic white patients (12%), suggesting a similar mutational frequency.    ///    To identify targetable biomarkers other than EGFR and EML4-ALK in Hispanic patients with lung adenocarcinoma.     ///    Our highly multiplexed genotyping assay detected actionable mutations in 14% (12 of 83) more patients than would have been identified by EGFR and EML4-ALK testing alone..     ///    \"Targetable biomarkers other than EGFR and EML4-ALK were identified in 7 of the 40 Hispanic patients (18%) and 5 of the 43 non-Hispanic white patients (12%), suggesting a similar mutational frequency. \"'), ('9957', 'NTRK3_ETV6', '', 'NTRK3', 'ETV6', '16681692', '0', 'nephoma\r\r', 'PCR;RT-PCR', 'Kinase', '', '', '', '', 'KB', 'Seq', 'two were non-informative and three expressed ETV6-NTRK3 using both techniques, two showing similar expression, whilst one showed expression two orders of magnitude lower, from a cellular tumour. '), ('9958', 'EML4_ALK', '', 'EML4', 'ALK', '21368458', '0', 'lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Transgenic mice expressing EML4-ALK in lung developed hundreds of lung cancer nodules soon after birth, but such nodules were readily eradicated upon treatment with an ALK inhibitor.    ///    \"Transgenic mice expressing EML4-ALK in lung developed hundreds of lung cancer nodules soon after birth, but such nodules were readily eradicated upon treatment with an ALK inhibitor. \"    ///    \"We have discovered a small, fusion-type tyrosine kinase EML4-ALK that is generated through a tiny inversion within the short arm of human chromosome 2. \"'), ('9959', 'PDGFRA_FIP1L1', '', 'PDGFRA', 'FIP1L1', '15175999', '0', 'endomyocardial fibrosis', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The efficacy of relatively low imatinib concentrations in HES, mediated by inhibition of FIP1L1-PDGFRalpha kinase activity, causally implicates FIP1L1-PDGFRA in the pathogenesis in certain HES patients.. '), ('9960', 'SCT_OGP', '', 'SCT', 'OGP', '16894884', '0', '', '', '', '', '', '', '', '', '', 'Finally, we got two stable SCT-OGP high expression clones after screening.     ///    [SCT-OGP fusion protein expression and its potential role as osteoporosis therapy].     ///    [SCT-OGP fusion protein expression and its potential role as osteoporosis therapy].. '), ('9961', 'SYT_SSX2', '', 'SYT', 'SSX2', '15364967', '0', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Median and 5-year metastasis-free survivals (MFS) were 84 months and 54.2% for SYT-SSX1 versus 50 months and 47.6% for SYT-SSX2 (P = .76).     ///    \"Among those patients with localized disease at diagnosis, median and 5-year disease-specific survivals (DSS) for the SYT-SSX1 and SYT-SSX2 subgroups were 126 months and 67.4% versus 82 months and 63.2%, respectively (P = .12). \"    ///    \"The following parameters were examined for their potential prognostic value: age at diagnosis, sex, tumor site (extremities v proximal/truncal), size, histology, mitotic count, necrosis, histologic grade (Federation Nationale des Centres de Lutte Contre le Cancer system), stage (1997 tumor-node-metastasis system classification), surgical margin status (assessed histologically), and fusion type (SYT-SSX1 v SYT-SSX2). \"'), ('9962', 'EML4_ALK', '', 'EML4', 'ALK', '24567430', '0', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Cost effectiveness of EML4-ALK fusion testing and first-line crizotinib treatment for patients with advanced ALK-positive non-small-cell lung cancer.    ///    Cost effectiveness of EML4-ALK fusion testing and first-line crizotinib treatment for patients with advanced ALK-positive non-small-cell lung cancer..     ///    EML4-ALK fusion testing in stage IV nonsquamous NSCLC with crizotinib treatment for ALK-positive patients is not cost effective in the setting of high drug costs and a low biomarker frequency in the population..     ///     ALK-targeted therapy with crizotinib offers significant improvement in clinical outcomes for the treatment of EML4-ALK fusion-positive non-small-cell lung cancer (NSCLC).     ///    We estimated the cost effectiveness of EML4-ALK fusion testing in combination with targeted first-line crizotinib treatment in Ontario. '), ('9963', 'KIF5B_RET', '', 'KIF5B', 'RET', '25349307', '0', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'In addition, alectinib showed kinase inhibitory activity against RET gatekeeper mutations (RET V804L and V804M) and blocked cell growth driven by the KIF5B-RET V804L and V804M.'), ('9964', 'PPFIBP1_ALK', '', 'PPFIBP1', 'ALK', '23957430', '0', '', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Inflammatory myofibroblastic tumour of the lung with a novel PPFIBP1-ALK fusion variant.. '), ('9965', 'STAT6_NAB2', '', 'STAT6', 'NAB2', '23575898', '0', 'solitary fibrous tumor\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', '', 'We performed exome sequencing and detected the NAB2-STAT6 fusion in DNA of 8/10 meningeal HPC thereby providing evidence of close relationship of these tumors with peripheral SFT.     ///    \"In conclusion, we provide strong evidence for meningeal HPC and SFT to constitute variants of a single entity which is defined by NAB2-STAT6 fusion. \"    ///    \"Recent detection of frequent NAB2-STAT6 fusions in both, HPC and SFT, provided additional support for this view. \"    ///    Meningeal hemangiopericytoma and solitary fibrous tumors carry the NAB2-STAT6 fusion and can be diagnosed by nuclear expression of STAT6 protein..     ///    \"More practical, presence of the NAB2-STAT6 fusion protein resulted in a strong nuclear signal in STAT6 immunohistochemistry. \"    ///    Tissues not harboring the NAB2-STAT6 fusion protein presented with nuclear expression of NAB2 and cytoplasmic expression of STAT6 proteins.     ///    \"Due to the considerable effort required for exome sequencing, we sought to explore surrogate markers for the NAB2-STAT6 fusion protein. \"    ///    We adopted the Duolink proximity ligation assay and demonstrated the presence of NAB2-STAT6 fusion protein in 17/17 HPC and the absence in 15/15 meningiomas.     ///    \"More practical, presence of the NAB2-STAT6 fusion protein resulted in a strong nuclear signal in STAT6 immunohistochemistry.\"'), ('9966', 'EML4_ALK', '', 'EML4', 'ALK', '25496960', '0', '', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Lung adenocarcinoma harboring concomitant EGFR mutation and EML4-ALK fusion that benefits from three kinds of tyrosine kinase inhibitors: a case report and literature review.. '), ('9967', 'EML4_ALK', '', 'EML4', 'ALK', '20855837', '0', 'adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Forty-one tumors harbored EGFR mutations, three harbored EML4-ALK fusions, two harbored HER2 insertions, and one harbored a KRAS mutation. '), ('9968', 'EWS_ERG', '', 'EWS', 'ERG', '9738976', '0', 'ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'EWS-FLI-1, EWS-ERG, EWS-ETV1 and EWS-FEV. '), ('9969', 'PPARG_PAX8', '', 'PPARG', 'PAX8', '16209039', '0', 'acute myeloid leukemia', '', '', '', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'PPARgamma and RARalpha are closely related members ofthe same nuclear receptor subfamily, and the PML-RARalpha and PAX8-PPARgamma fusion proteins both function as dominant negative inhibitors of their wild-type parent proteins. '), ('9970', 'EML4_ALK', '', 'EML4', 'ALK', '25669975', '0', 'cervical cancer;squamous cell carcinoma', 'PCR;RT-PCR', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'No mutations were detected in AKT1 or BRAF, and the fusions FGFR1-TACC1, EML4-ALK, CCDC6-RET and KIF5B-RET were not found in any of the cancers.    ///    \"No mutations were detected in AKT1 or BRAF, and the fusions FGFR1-TACC1, EML4-ALK, CCDC6-RET and KIF5B-RET were not found in any of the cancers. \"'), ('9971', 'EML4_ALK', '', 'EML4', 'ALK', '24900831', '0', '', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Compound 8a displayed appreciable antitumor efficacy at the dose of 1 mg/kg in the ALK-driven BF3/EML4-ALK xenograft mice model.'), ('9972', 'EML4_ALK', '', 'EML4', 'ALK', '23423768', '0', 'squamous cell carcinoma', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The two essential requirements for pathologic specimens in the era of personalized therapies for non-small cell lung carcinoma (NSCLC) are accurate subtyping as adenocarcinoma (ADC) versus squamous cell carcinoma (SqCC) and suitability for EGFR molecular testing, as well as for testing of other oncogenes such as EML4-ALK and KRAS.    ///    \" The two essential requirements for pathologic specimens in the era of personalized therapies for non-small cell lung carcinoma (NSCLC) are accurate subtyping as adenocarcinoma (ADC) versus squamous cell carcinoma (SqCC) and suitability for EGFR molecular testing, as well as for testing of other oncogenes such as EML4-ALK and KRAS. \"'), ('9973', 'ZNF198_FGFR1', 't(8;13)(p11;q12) / t(8;13)  / ', 'ZNF198', 'FGFR1', '10643154', '0', 'myeloproliferative disorder;non Hodgkin lymphoma;leukemia;lymphoma\r\r', '', 'Kinase', '', '', '', '', 'KB', '', 'Not the BCR/ABL, but the ZNF198/FGFR1 chimeric mRNA was detected by reverse transcription-polymerase chain reaction. '), ('9974', 'EML4_ALK', '', 'EML4', 'ALK', '25501361', '0', 'non small cell lung cancer;lung cancer;adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'We retrospectively analyzed patients with EML4-ALK positive advanced NSCLC who were treated with crizotinib from May 2012 to Aug 2013.    ///    We retrospectively analyzed patients with EML4-ALK positive advanced NSCLC who were treated with crizotinib from May 2012 to Aug 2013.     ///    The EML4-ALK fusion rate and number of prior chemotherapy cycles did not appear to significantly affect the efficacy of crizotinib. '), ('9975', 'KIAA1549_BRAF', '', 'KIAA1549', 'BRAF', '23831947', '0', 'gliomatosis cerebri', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'However, KIAA1549-BRAF fusion characterizes pilocytic astrocytomas whereas V600E BRAF mutation is mainly recorded in pleomorphic xanthoastrocytomas and gangliogliomas.    ///    \"However, KIAA1549-BRAF fusion characterizes pilocytic astrocytomas whereas V600E BRAF mutation is mainly recorded in pleomorphic xanthoastrocytomas and gangliogliomas. \"'), ('9976', 'RET_ELE1', '', 'RET', 'ELE1', '16209039', '0', 'acute myeloid leukemia', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'In fact, the ELE1-RET (PTC3) fusion protein contains the ELE1 nuclear receptor co-activator domain and it appears to physically associate with and inhibit wild-type PPARgamma in some papillary carcinomas. '), ('9977', 'EML4_ALK', '', 'EML4', 'ALK', '23154565', '0', 'small cell lung cancer;lung cancer;adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'First case of combined small-cell lung cancer with adenocarcinoma harboring EML4-ALK fusion and an exon 19 EGFR mutation in each histological component.. '), ('9978', 'BCR_ABL1', '', 'BCR', 'ABL1', '21641037', '0', 'chronic myeloid leukemia;myeloid leukemia;leukemia\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Molecular response to first line nilotinib in a patient with e19a2 BCR-ABL1 chronic myeloid leukemia.. '), ('9979', 'MLL_GRAF', '', 'MLL', 'GRAF', '15852479', '0', 'acute myeloid leukemia', '', '', '', '', '', '', '', '', 'Use of MLL/GRAF fusion mRNA for measurement of minimal residual disease during chemotherapy in an infant with acute monoblastic leukemia (AML-M5).. '), ('9980', 'TEL_AML1', '', 'TEL', 'AML1', '10687723', '0', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'Therefore, TEL-AML1 fusion confers a favorable prognosis in some protocols of chemotherapy but not in others. '), ('9981', 'EWSR1_ATF1', '', 'EWSR1', 'ATF1', '24595418', '0', 'cystadenocarcinoma', '', '', '', '', '', 'Transcription_Factor', 'KB', 'Seq', 'The EWSR1-ATF1 fusion is specific for HCCC within the context of salivary neoplasia.    ///    The EWSR1-ATF1 fusion is specific for HCCC within the context of salivary neoplasia. '), ('9982', 'SYT_SSX1', '', 'SYT', 'SSX1', '15364967', '0', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Among those patients with localized disease at diagnosis, median and 5-year disease-specific survivals (DSS) for the SYT-SSX1 and SYT-SSX2 subgroups were 126 months and 67.4% versus 82 months and 63.2%, respectively (P = .12).     ///    Median and 5-year metastasis-free survivals (MFS) were 84 months and 54.2% for SYT-SSX1 versus 50 months and 47.6% for SYT-SSX2 (P = .76).     ///    \"The following parameters were examined for their potential prognostic value: age at diagnosis, sex, tumor site (extremities v proximal/truncal), size, histology, mitotic count, necrosis, histologic grade (Federation Nationale des Centres de Lutte Contre le Cancer system), stage (1997 tumor-node-metastasis system classification), surgical margin status (assessed histologically), and fusion type (SYT-SSX1 v SYT-SSX2). \"'), ('9983', 'FEV_EWS', '', 'FEV', 'EWS', '9738976', '0', 'ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'EWS-FLI-1, EWS-ERG, EWS-ETV1 and EWS-FEV. '), ('9984', 'EML4_ALK', '', 'EML4', 'ALK', '23277484', '0', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'EML4-ALK, PIK3CA, and MEK1 mutations occurred in NSCLC with various distinct clinicopathological characteristics.     ///    \"EML4-ALK, PIK3CA, and MEK1 mutations were mutually exclusive. \"    ///    \"EML4-ALK, PIK3CA, and MEK1 mutations were mutually exclusive.\"    ///    \"Furthermore, tumors with EML4-ALK fusions had significantly higher levels of ERCC1, a molecule with a key role in platinum drug efficacy, than tumors without EML4-ALK fusions. \"    ///    EML4-ALK fusion was found to be of coexistence with EGFR and KRAS mutations in two cases.     ///    EML4-ALK fusions could serve as a significant prognostic indicator for locally advanced NSCLC..     ///    \"Moreover, multivariate analysis indicated that in stage IIIA NSCLC EML4-ALK fusion was the only significant indicator for poor DFS (P < 0.001). \"    ///    \"Of 488 patients with NSCLC, 28 had EML4-ALK fusions. \"    ///    \"Furthermore, tumors with EML4-ALK fusions had significantly higher levels of ERCC1, a molecule with a key role in platinum drug efficacy, than tumors without EML4-ALK fusions.\"'), ('9985', 'NUP98_HOXD13', '', 'NUP98', 'HOXD13', '17377591', '0', 'chronic myeloid leukemia;myeloid leukemia;myelodysplastic syndrome;leukemia\r\r', '', '', 'Oncogene', '', '', '', 'KB', 'Seq', ' NUP98-HOXD13 (NHD13) fusions have been identified in patients with myelodysplastic syndrome, acute myelogenous leukemia and chronic myeloid leukemia blast crisis.     ///    Mouse embryonic stem cells that express a NUP98-HOXD13 fusion protein are impaired in their ability to differentiate and can be complemented by BCR-ABL.. '), ('9986', 'EML4_ALK', '', 'EML4', 'ALK', '23559882', '0', 'renal cell carcinoma;non small cell lung cancer;colorectal cancer;small\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Those agents range from improved cytotoxics such as pemetrexed, to targeted therapies such as tyrosine kinase inhibitors of the epidermal growth factor receptor and agents that target the EML4-ALK gene mutation.    ///    \"Those agents range from improved cytotoxics such as pemetrexed, to targeted therapies such as tyrosine kinase inhibitors of the epidermal growth factor receptor and agents that target the EML4-ALK gene mutation. \"'), ('9987', 'MBP_PLP', '', 'MBP', 'PLP', '16781782', '0', '', '', '', '', '', '', '', '', '', 'MBP-PLP fusion protein-induced EAE in C57BL/6 mice.     ///    MBP-PLP fusion protein-induced EAE in C57BL/6 mice..     ///    Here we are introducing MBP-PLP fusion protein (MP4)-induced EAE for C57BL/6 mice. '), ('9988', 'PAX3_FOXO1', '', 'PAX3', 'FOXO1', '24334454', '0', 'rhabdomyosarcoma;sarcoma\r\r', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', 'KB', 'Seq', 'Previously, we reported that PAX3-FOXO1 supports aRMS initiation by enabling bypass of cellular senescence checkpoints.    ///    \"Despite its discovery nearly two decades ago, the mechanisms by which PAX3-FOXO1 drives tumor development are not well characterized. \"    ///    \"Additionally, we identify a mechanism used by PAX3-FOXO1 to inhibit MST1 signaling and promote tumorigenesis in aRMS. \"    ///    Alveolar rhabdomyosarcoma-associated PAX3-FOXO1 promotes tumorigenesis via Hippo pathway suppression..     ///    \"Previously, we reported that PAX3-FOXO1 supports aRMS initiation by enabling bypass of cellular senescence checkpoints. \"    ///     Alveolar rhabdomyosarcoma (aRMS) is an aggressive sarcoma of skeletal muscle characterized by expression of the paired box 3-forkhead box protein O1 (PAX3-FOXO1) fusion oncogene. '), ('9989', 'PBX1_E2A', 't(1;19)  / ', 'PBX1', 'E2A', '24503810', '0', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia\r\r', '', '', '', '', '', 'Transcription_Factor', '', '', 'The E2A-PBX1 chimeric transcription factor contains the N-terminal transactivation domain of E2A (TCF3) fused to the C-terminal DNA-binding homeodomain of PBX1. '), ('9990', 'EML4_ALK', '', 'EML4', 'ALK', '23098378', '0', 'adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'In this series, 230 resected lung adenocarcinomas from smoker (>100 cigarettes in lifetime) at single center (Shanghai Cancer Center, Shanghai, China) were tested for mutation in EGFR, KRAS, BRAF, HER2, EML4-ALK and PIK3CA.     ///    \"Among 230 smokers, we detected 100 (43.5%) EGFR mutations, 38 (16.5%) KRAS mutations, 8 (3.5%) PIK3CA mutations, 7 (3.0%) BRAF mutations and 7 (3.0%) EML4-ALK fusions. \"'), ('9991', 'TMPRSS2_ERG', '', 'TMPRSS2', 'ERG', '18794177', '0', 'prostate cancer\r\r', 'PCR;RT-PCR', '', '', '', '', '', 'KB', 'Seq', 'Among all of the reported fusion partners in the ETS gene family, TMPRSS2:ERG is the most prevalent one. '), ('9992', 'TMPRSS2_ERG', '', 'TMPRSS2', 'ERG', '25520876', '0', 'prostate cancer\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'However, samples with a CAG repeat of 17 were found more frequently in the TMPRSS2:ERG fusion positive than negative prostate cancer cases and mediated a higher rate of androgen-induced TMPRSS2 and ERG co-localisation than AR with longer (24) and shorter (15) CAG repeats.    ///    \"However, samples with a CAG repeat of 17 were found more frequently in the TMPRSS2:ERG fusion positive than negative prostate cancer cases and mediated a higher rate of androgen-induced TMPRSS2 and ERG co-localisation than AR with longer (24) and shorter (15) CAG repeats. \"    ///    \"Shorter CAG repeat length was also not shown to be associated with a higher induction rate of TMPRSS2 and ERG proximity, an essential step for TMPRSS2:ERG fusion formation. \"'), ('9993', 'RET_KIF5B', '', 'RET', 'KIF5B', '22327623', '0', 'lung cancer;adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'In addition, we discovered previously unidentified kinase fusions that may be promising for molecular-targeted therapy, kinesin family member 5B (KIF5B)-ret proto-oncogene (RET) and coiled-coil domain containing 6 (CCDC6)-RET, in 14 adenocarcinomas. '), ('9994', 'MLL_ENL', '', 'MLL', 'ENL', '16688745', '0', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'We have tested this idea by exploiting a hormone regulated MLL-ENL (MLLT1) activation system and show that MLL-ENL function in normal murine progenitor cells substantially increases the incidence of chromosomal abnormalities in proliferating cells that survive exposure to etoposide VP-16. '), ('9995', 'EWS_CHOP', 't(12;16)(q13;p11) / ', 'EWS', 'CHOP', '8637704', '0', 'liposarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'The presence of the EWS/CHOP chimeric gene in MLS shows that (i) the N-terminal part of FUS may be replaced by the N-terminal part of EWS in a CHOP fusion oncoprotein (ii) the two N-terminal parts, when fused to certain transcription factors, have a common or very similar oncogenic potential and (iii) the tumorigenic process in MLS and the morphogenetically distinctly different EWS-associated tumor types may be related..     ///    \"The result was a fusion of the N-terminal part of the EWS gene in 22q12, involved in a number of mesenchymal tumor types, with the CHOP gene and the creation of an EWS/CHOP chimeric gene. \"'), ('9996', 'EML4_ALK', '', 'EML4', 'ALK', '22056890', '0', '', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Successful long-term treatment with pemetrexed of NSCLC associated with EML4-ALK and low thymidylate synthase expression.    ///    Successful long-term treatment with pemetrexed of NSCLC associated with EML4-ALK and low thymidylate synthase expression.. '), ('9997', 'KIAA1549_BRAF', '', 'KIAA1549', 'BRAF', '25524464', '0', 'ganglioglioma', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Activation of the MAP Kinase (MAPK) pathway caused by the BRAFV600E mutation or the KIAA1549-BRAF fusion has been reported in pediatric GG and PA, respectively.    ///    \"Activation of the MAP Kinase (MAPK) pathway caused by the BRAFV600E mutation or the KIAA1549-BRAF fusion has been reported in pediatric GG and PA, respectively. \"'), ('9998', 'EML4_ALK', '', 'EML4', 'ALK', '25393796', '0', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'This patient and another patient with EML4-ALK variant 3a/b initially responded sequentially to crizotinib and then alectinib, a next-generation ALK inhibitor, but developed acquired resistance to alectinib with the presence of a mutation in amino acid residue 1171 (I1171N and I1171S respectively) located in the hydrophobic regulatory spine (R-spine) of the ALK kinase in both the cases as identified by a comprehensive next-generation sequencing-based assay performed on biopsies of new liver metastases that developed during alectinib treatment.     ///    \"This patient and another patient with EML4-ALK variant 3a/b initially responded sequentially to crizotinib and then alectinib, a next-generation ALK inhibitor, but developed acquired resistance to alectinib with the presence of a mutation in amino acid residue 1171 (I1171N and I1171S respectively) located in the hydrophobic regulatory spine (R-spine) of the ALK kinase in both the cases as identified by a comprehensive next-generation sequencing-based assay performed on biopsies of new liver metastases that developed during alectinib treatment.\"'), ('9999', 'EML4_ALK', '', 'EML4', 'ALK', '25612681', '0', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The discovery of driver oncogene alterations in non-small cell lung cancer (NSCLC), such as EGFR, EML4-ALK, MET and RAS, as well as the identification of their specific targeted inhibitors have led to new opportunities for treatment of this tumor.    ///    \" The discovery of driver oncogene alterations in non-small cell lung cancer (NSCLC), such as EGFR, EML4-ALK, MET and RAS, as well as the identification of their specific targeted inhibitors have led to new opportunities for treatment of this tumor. \"'), ('10000', 'EML4_ALK', '', 'EML4', 'ALK', '26107243', '0', 'non small cell lung cancer', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'A Pooled Analysis on Crizotinib in Treating Chinese Patients with EML4-ALK Positive Non-small-cell Lung Cancer.    ///    This pooled analysis suggests that crizotinib based regimens are associated with good response rate and accepted toxicities in treating Chinese patients with EML4-ALK positive non-small-cell lung cancer..     ///    Clinical studies evaluating the efficacy and safety of crizotinib based regimens on response and safety for Chinese patients with EML4-ALK positive non-small-cell lung cancer were identified by using a predefined search strategy.     ///     This analysis was conducted to evaluate the efficacy and safety of crizotinib based regimens in treating Chinese patients with EML4-ALK positive non-small-cell lung cancer.     ///    \"In crizotinib based regimens, 3 clinical studies which including 128 Chinese patients with EML4-ALK positive non-small-cell lung cancer and treated with crizotinib based regimen were considered eligible for inclusion. \"    ///    A Pooled Analysis on Crizotinib in Treating Chinese Patients with EML4-ALK Positive Non-small-cell Lung Cancer.. '), ('10001', 'EML4_ALK', '', 'EML4', 'ALK', '24200637', '0', 'non small cell lung cancer;colorectal cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'A second NSCLC patient showed an EML4-ALK fusion with ALK, EGFR, and MET mutations.    ///    \"A second NSCLC patient showed an EML4-ALK fusion with ALK, EGFR, and MET mutations. \"'), ('10002', 'NAB2_STAT6', '', 'NAB2', 'STAT6', '26425382', '0', 'solitary fibrous tumor\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', '', 'Importance of NAB2-STAT6 Fusion in the Diagnosis of Pancreatic Solitary Fibrous Tumor with Hamartoma-Like Features: A Case Report and Review of the Literature.    ///    \"Thus, we evaluated NAB2-STAT6 fusion. \"    ///    \" We report a case of pancreatic hamartoma-like solitary fibrous tumor which was differentiated from pancreatic hamartoma with the detection of NAB2-STAT6 fusion, a specific mutation for solitary fibrous tumors. \"    ///    Importance of NAB2-STAT6 Fusion in the Diagnosis of Pancreatic Solitary Fibrous Tumor with Hamartoma-Like Features: A Case Report and Review of the Literature..     ///    \"In conclusion, detection of NAB2-STAT6 fusion has a great diagnostic value for pancreatic solitary fibrous tumors with hamartoma-like features. \"'), ('10003', 'EML4_ALK', '', 'EML4', 'ALK', '22317764', '0', 'adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Two hundred and sixty-six (76.2%) tumors harbored EGFR mutations, 16 (4.6%) HER2 mutations, 15 (4.3%) EML4-ALK fusions, seven (2.0%) KRAS mutations, and two (0.6%) BRAF mutations.     ///    \"Two hundred and sixty-six (76.2%) tumors harbored EGFR mutations, 16 (4.6%) HER2 mutations, 15 (4.3%) EML4-ALK fusions, seven (2.0%) KRAS mutations, and two (0.6%) BRAF mutations.\"'), ('10004', 'ATIC_ALK', '', 'ATIC', 'ALK', '17464320', '0', 'anaplastic large cell lymphoma;lymphoma\r\r', 'PCR;RT-PCR', 'Kinase', 'Oncogene', '', '', '', 'KB', '', 'The 5\' RACE assay detected ATIC-ALK fusion in the remaining case. '), ('10005', 'ETV6_JAK2', '', 'ETV6', 'JAK2', '20507304', '0', 'myeloproliferative disorder\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', '', 'The compound also demonstrated significant therapeutic potential in vivo in an ETV6-JAK2 (TEL-JAK2) murine leukaemia model.    ///    The compound also demonstrated significant therapeutic potential in vivo in an ETV6-JAK2 (TEL-JAK2) murine leukaemia model. '), ('10006', 'PAX8_PPARG', '', 'PAX8', 'PPARG', '24025583', '0', 'thyroid carcinoma;thyloid cancer\r\r', '', '', '', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'A chromosomal translocation results in the production of a paired box 8-peroxisome proliferator-activated receptor gamma (PAX8-PPARG) fusion protein (PPFP) in ?35% of follicular thyroid carcinomas.    ///    The thyroid cancer PAX8-PPARG fusion protein activates Wnt/TCF-responsive cells that have a transformed phenotype.'), ('10007', 'NR4A3_EWSR1', '', 'NR4A3', 'EWSR1', '18855877', '-1', 'chondrosarcoma;sarcoma\r\r', '', '', '', '', 'Receptor', 'Transcription_Factor', 'KB', '', 'Bioinformatic analysis identified a DNA response element for EWSR1/NR4A3 in the PPARG promoter, and band-shift experiments and transient transfections indicate that EWSR1/NR4A3 can activate transcription through this element.     ///    \"These results suggest that the overall expression of PPARG in EMC may be regulated in part by the balance between EWSR1/NR4A3 and NR4A3, and that PPARG may play a crucial role in the development of these tumours. \"    ///    Western blot or immunohistochemical analyses confirm that PPARG and NDRG2 are expressed in tumours positive for EWSR1/NR4A3.     ///    The specific up-regulation of PPARG by EWSR1/NR4A3 may also have potential therapeutic implications..     ///    The EWSR1/NR4A3 fusion protein of extraskeletal myxoid chondrosarcoma activates the PPARG nuclear receptor gene.    ///    \"We performed an expression microarray analysis of EMC tumours expressing the EWSR1/NR4A3 fusion protein, comparing their expression profiles to those of other sarcoma types.\"    ///    \"Western blots further show that an isoform of the native NR4A3 receptor lacking the C-terminal domain is very highly expressed in tumours positive for EWSR1/NR4A3, and co-transfections of this isoform along with EWSR1/NR4A3 indicate that it may negatively regulate the activity of the fusion protein on the PPARG promoter. \"    ///    \"We performed an expression microarray analysis of EMC tumours expressing the EWSR1/NR4A3 fusion protein, comparing their expression profiles to those of other sarcoma types. \"    ///    The EWSR1/NR4A3 fusion protein of extraskeletal myxoid chondrosarcoma activates the PPARG nuclear receptor gene.. '), ('10008', 'TAF2N_CHN', '', 'TAF2N', 'CHN', '16220270', '-1', 'chondrosarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Fusion gene transcripts could be detected in 13 (68%) of the 19 cases: EWS-CHN in nine cases, TAF2N-CHN in three, and TFG-TCH in one.     ///    \"All cases with TAF2N-CHN or TFG-TCH variants showed invasion of extracompartmental structure, bone, or vessels. \"'), ('10009', 'SYT_SSX2', '', 'SYT', 'SSX2', '11720441', '-1', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'However, we could not confirm the prediction value of the biphasic subtype for the presence of the SYT-SSX1 transcript since in our hands 6 out 33 (18%) biphasic tumours carried the SYT-SSX2 transcript.. '), ('10010', 'FLI1_EWSR1', '', 'FLI1', 'EWSR1', '26056084', '-1', 'ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', 'Seq', 'Trabectedin is an antitumoral agent that modulates EWSR1-FLI1 transcriptional functions, causing DNA damage.     ///    \"Interestingly, PARP1 is also a transcriptional regulator of EWSR1-FLI1, and PARPinh disrupts the DDR machinery. \"    ///    \"The drug combination also enhanced ?H2AX intranuclear accumulation as a result of DNA damage induction, DNA fragmentation and global DDR deregulation, while EWSR1-FLI1 target expression remained unaffected.\"    ///    \"Thus, given the impact and apparent specificity of both agents with regard to the DNA damage/DDR system and EWSR1-FLI1 activity in ES, we decided to explore the activity of combining PARPinh and Trabectedin in in vitro and in vivo experiments. \"    ///    \"The drug combination also enhanced ?H2AX intranuclear accumulation as a result of DNA damage induction, DNA fragmentation and global DDR deregulation, while EWSR1-FLI1 target expression remained unaffected. \"'), ('10011', 'EWSR1_DDIT3', '', 'EWSR1', 'DDIT3', '26595521', '-1', 'liposarcoma;sarcoma\r\r', '', '', '', '', '', 'Transcription_Factor', 'KB', '', 'MLS is characterized by the FUS-DDIT3 or EWSR1-DDIT3 fusion oncogenes that encode abnormal transcription factors.'), ('10012', 'NPM1_ALK', '', 'NPM1', 'ALK', '17922009', '-1', '', '', 'Kinase', 'Oncogene', '', '', 'Transcription_Factor', 'KB', 'Seq', 'The DNA methylation is induced by NPM1-ALK itself via STAT3, and is associated with binding to the promoter of the gene encoding MeCP2 capping protein and with lack of binding of the STAT5A gene transcription activator SP1.     ///    STAT5A is epigenetically silenced by the tyrosine kinase NPM1-ALK and acts as a tumor suppressor by reciprocally inhibiting NPM1-ALK expression.    ///    Here we report that STAT5A expression is selectively inhibited by DNA methylation of the STAT5A gene promoter region in cells expressing the oncogenic tyrosine kinase NPM1-ALK (also known as NPM-ALK).     ///    STAT5A is epigenetically silenced by the tyrosine kinase NPM1-ALK and acts as a tumor suppressor by reciprocally inhibiting NPM1-ALK expression..     ///    These results show that NPM1-ALK induces epigenetic silencing of STAT5A gene and that STAT5A protein can act as a key tumor suppressor by reciprocally inhibiting expression of NPM1-ALK..     ///    \"Notably, the induced or exogenously expressed STAT5A protein binds to the enhancer and intron 14 of the NPM1-ALK gene and triggers selective suppression of NPM1-ALK expression. \"'), ('10013', 'BCR_ABL1', '', 'BCR', 'ABL1', '24109527', '-1', 'bone marrow fibrosis\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', ' A minority of chronic myeloid leukaemia (CML) patients express variant transcripts of which the e19a2 BCR-ABL1 fusion is the most common.     ///    Rapid Evolution to Blast Crisis Associated with a Q252H ABL1 Kinase Domain Mutation in e19a2 BCR-ABL1 Chronic Myeloid Leukaemia..     ///    \"A case of e19a2 BCR-ABL1 CML is described in whom imatinib resistance, associated with a Q252H ABL1 kinase domain mutation, became apparent soon after initiation of TKI therapy. \"    ///    Instances of tyrosine kinase inhibitor (TKI) resistance in e19a2 BCR-ABL1 CML patients have rarely been reported.     ///    This scenario of Q252H-associated TKI resistance with rapid BC transformation has not been previously documented in e19a2 BCR-ABL1 CML. '), ('10014', 'CRTC1_MAML2', '', 'CRTC1', 'MAML2', '19644446', '-1', '', '', '', '', '', '', 'Transcription_Factor', 'KB', 'Seq', 'Interestingly, the CRTC1-MAML2 oncoprotein lacks the splicing domain and is incapable of altering splice-site selection despite robustly activating transcription.    ///    \"Interestingly, the CRTC1-MAML2 oncoprotein lacks the splicing domain and is incapable of altering splice-site selection despite robustly activating transcription. \"'), ('10015', 'KIAA1549_BRAF', '', 'KIAA1549', 'BRAF', '26222501', '-1', 'pilocytic astrocytoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'We used reverse transcription polymerase chain reaction for the 3 most common KIAA1549-BRAF fusions, together with BRAF V600E and histone H3.3 K27M analyses to identify relationships of these molecular characteristics with clinical features in a cohort of 32 PA patients.     ///    Pilocytic astrocytomas (PAs) are increasingly tested for KIAA1549-BRAF fusions.    ///     Pilocytic astrocytomas (PAs) are increasingly tested for KIAA1549-BRAF fusions.     ///    \"Thus, in this small cohort, 15-9 KIAA1549-BRAF fusion was associated with midline PAs located outside of the cerebellum. \"    ///    BRAF Fusion Analysis in Pilocytic Astrocytomas: KIAA1549-BRAF 15-9 Fusions Are More Frequent in the Midline Than Within the Cerebellum.. '), ('10016', 'EWS_ERG', '', 'EWS', 'ERG', '7599072', '-1', '', '', '', '', '', '', '', '', '', 'EWS/FLI-1 and EWS/ERG transcripts being observed in eight and two cases respectively. '), ('10017', 'SYT_SSX2', '', 'SYT', 'SSX2', '16849535', '-1', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'We report here that SYT-SSX1 and SYT-SSX2 interact preferentially with Snail or Slug, respectively, and prevent these transcriptional repressors from binding to the proximal E-cadherin promoter as shown by coimmunoprecipitation and chromatin immunoprecipitation.     ///    Luciferase reporter assays reveal that SYT-SSX1 and SYT-SSX2 can respectively overcome the Snail- or Slug-mediated repression of E-cadherin transcription.     ///    \"The striking spontaneous mesenchymal to epithelial differentiation in this cancer is reminiscent of a developmental switch, but the only clue to its mechanistic basis has been the observation that most cases of synovial sarcoma with glandular epithelial differentiation (GED) contain SYT-SSX1 instead of SYT-SSX2. \"    ///    SYT-SSX1 and SYT-SSX2 interfere with repression of E-cadherin by snail and slug: a potential mechanism for aberrant mesenchymal to epithelial transition in human synovial sarcoma.. '), ('10018', 'BCR_ABL1', '', 'BCR', 'ABL1', '21072049', '-1', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The first case of acute lymphoblastic leukemia with the e19a2 BCR-ABL1 transcript: imatinib therapy followed by unrelated donor transplantation induces a durable molecular response.. '), ('10019', 'EML4_ALK', '', 'EML4', 'ALK', '24183104', '-1', 'non small cell lung cancer;lung cancer;adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'For lung cancer patients with positive brushing cytology, analysis of EGFR, K-ras and EML4-ALK fusions were carried out, utilizing reverse transcription-polymerase chain reaction and Sanger sequencing on the cell-derived RNA retrieved from waste brushing samples.     ///    \"Of the 19 patients with adenocarcinoma or non-small cell lung cancer not otherwise specified harboring wild-type EGFR and K-ras, two cases (10.5%) were identified to harbor EML4-ALK fusions. \"'), ('10020', 'BCR_ABL1', '', 'BCR', 'ABL1', '19136943', '-1', 'prostate cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'As a proof of concept, we successfully used integrative transcriptome sequencing to \'re-discover\' the BCR-ABL1 (ref. '), ('10021', 'EWSR1_FLI1', '', 'EWSR1', 'FLI1', '26214589', '-1', 'ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'Ewing sarcoma is characterized by fusions between EWSR1 and members of the ETS gene family, usually EWSR1-FLI1, leading to the generation of oncogenic transcription factors that bind DNA at GGAA motifs.    ///    \"Ewing sarcoma is characterized by fusions between EWSR1 and members of the ETS gene family, usually EWSR1-FLI1, leading to the generation of oncogenic transcription factors that bind DNA at GGAA motifs. \"    ///    Chimeric EWSR1-FLI1 regulates the Ewing sarcoma susceptibility gene EGR2 via a GGAA microsatellite.    ///    \"EWSR1-FLI1 preferentially bound to the A risk allele, which increased global and allele-specific EGR2 expression. \"    ///    Chimeric EWSR1-FLI1 regulates the Ewing sarcoma susceptibility gene EGR2 via a GGAA microsatellite.. '), ('10022', 'SYT_SSX1', '', 'SYT', 'SSX1', '16849535', '-1', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'We report here that SYT-SSX1 and SYT-SSX2 interact preferentially with Snail or Slug, respectively, and prevent these transcriptional repressors from binding to the proximal E-cadherin promoter as shown by coimmunoprecipitation and chromatin immunoprecipitation.     ///    Luciferase reporter assays reveal that SYT-SSX1 and SYT-SSX2 can respectively overcome the Snail- or Slug-mediated repression of E-cadherin transcription.     ///    \"The striking spontaneous mesenchymal to epithelial differentiation in this cancer is reminiscent of a developmental switch, but the only clue to its mechanistic basis has been the observation that most cases of synovial sarcoma with glandular epithelial differentiation (GED) contain SYT-SSX1 instead of SYT-SSX2. \"    ///    SYT-SSX1 and SYT-SSX2 interfere with repression of E-cadherin by snail and slug: a potential mechanism for aberrant mesenchymal to epithelial transition in human synovial sarcoma..     ///    \"A subset of synovial sarcoma, predominantly cases with the SYT-SSX1 fusion, shows foci of morphologic epithelial differentiation in the form of nests of glandular epithelium. \"    ///    \"This provides a mechanism by which E-cadherin expression, a prerequisite of epithelial differentiation, is aberrantly derepressed in synovial sarcoma and may also explain the association of GED with the SYT-SSX1 fusion because it interferes with Snail, the stronger repressor of the E-cadherin promoter. \"'), ('10023', 'EWS_CHN', '', 'EWS', 'CHN', '16220270', '-1', 'chondrosarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Fusion gene transcripts could be detected in 13 (68%) of the 19 cases: EWS-CHN in nine cases, TAF2N-CHN in three, and TFG-TCH in one.     ///    Peripheral enhancement was seen more frequently in tumors with the EWS-CHN variant than in those with other cytogenetic variants. '), ('10024', 'EWSR1_FLI1', '', 'EWSR1', 'FLI1', '25031013', '-1', 'olfactory neuroblastoma', '', '', '', '', '', '', 'KB', 'Seq', 'A recent study using a limited number of tumor samples has shown that NKX2.2, a putative transcriptional target of EWSR1-FLI1, is a useful marker for the diagnosis of ES.    ///    \"A recent study using a limited number of tumor samples has shown that NKX2.2, a putative transcriptional target of EWSR1-FLI1, is a useful marker for the diagnosis of ES. \"    ///    \"The combination of CD99 and NKX2.2, a transcriptional target of EWSR1-FLI1, is highly specific for the diagnosis of Ewing sarcoma.. \"    ///    \"In the present study, the immunohistochemical expression of NKX2.2 was evaluated on 46 genetically confirmed ES and 85 non-ES SRCTs, together with comparative assessment of CD99 and other molecular targets of EWSR1-FLI1, including NR0B1, E2F3, and EZH2. \"'), ('10025', 'MAML2_CRTC3', '', 'MAML2', 'CRTC3', '21668476', '-1', 'mucoepidermoid carcinoma\r\r', '', '', '', '', '', 'Transcription_Factor', '', '', 'MEC cases (n = 111) were screened for CRTC1-MAML2 and CRTC3-MAML2 fusions by reverse transcription polymerase chain reaction.     ///    and the presence of CRTC1-MAML2 or CRTC3-MAML2 fusions.     ///     The aim of study was to evaluate the impact of CRTC1-MAML2 and CRTC3-MAML2 fusions on the histological classification of mucoepidermoid carcinoma (MEC) of the salivary glands and on the prognosis of patients.     ///    MEC cases positive for CRTC1-MAML2 or CRTC3-MAML2 fusion formed a favourable tumour subset that was distinct from fusion-negative cases. '), ('10026', 'MAML2_CRTC1', '', 'MAML2', 'CRTC1', '21668476', '-1', 'mucoepidermoid carcinoma\r\r', '', '', '', '', '', 'Transcription_Factor', 'KB', 'Seq', 'MEC cases (n = 111) were screened for CRTC1-MAML2 and CRTC3-MAML2 fusions by reverse transcription polymerase chain reaction.     ///     The aim of study was to evaluate the impact of CRTC1-MAML2 and CRTC3-MAML2 fusions on the histological classification of mucoepidermoid carcinoma (MEC) of the salivary glands and on the prognosis of patients.     ///    MEC cases positive for CRTC1-MAML2 or CRTC3-MAML2 fusion formed a favourable tumour subset that was distinct from fusion-negative cases.     ///    and the presence of CRTC1-MAML2 or CRTC3-MAML2 fusions. '), ('10027', 'EML4_ALK', '', 'EML4', 'ALK', '18166835', '-1', 'squamous cell carcinoma', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Using reverse transcription-polymerase chain reaction for EML4-ALK fusion mRNA, we investigated 149 lung adenocarcinomas, 48 squamous cell carcinomas, 3 large-cell neuroendocrine carcinomas, and 21 small-cell carcinomas.     ///    \"Using reverse transcription-polymerase chain reaction for EML4-ALK fusion mRNA, we investigated 149 lung adenocarcinomas, 48 squamous cell carcinomas, 3 large-cell neuroendocrine carcinomas, and 21 small-cell carcinomas.\"    ///    \"Herein, we present results of a first large scale study of EML4-ALK fusion in lung cancers. \"    ///    \"Five of 149 adenocarcinomas (3.4%) showed EML4-ALK fusion mRNA, this being totally lacking in carcinomas of other types (0/72). \"    ///    EML4-ALK fusion is linked to histological characteristics in a subset of lung cancers..     ///    The five fusion cases featured two EML4-ALK variant 1 fusions and three variant 2 fusions.     ///    \"In the present first investigation of EML4-ALK fusion in a large study of lung cancers (5/221), we found an interesting histotype-genotype relationship. \"    ///    Tumors featuring EML4-ALK fusion constitute one subtype of NSCLC that might be highly sensitive to ALK inhibitors.     ///    \"Five of 149 adenocarcinomas (3.4%) showed EML4-ALK fusion mRNA, this being totally lacking in carcinomas of other types (0/72).\"'), ('10028', 'KIAA1549_BRAF', '', 'KIAA1549', 'BRAF', '21518014', '-1', 'pilocytic astrocytoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'To evaluate at molecular level potential affinities between these tumors, we investigated a case of RGNT, arising in the cerebellum of a young patient, for the presence of transcriptional products originating from the KIAA1549-BRAF fusion.     ///    Further studies in larger RGNT case series are needed in order to demonstrate the possible presence of KIAA1549-BRAF fusion and better delineate its relationship with pilocytic astrocytomas..     ///    Analysis of KIAA1549-BRAF fusion status in a case of rosette-forming glioneuronal tumor of the fourth ventricle (RGNT).. ');
INSERT INTO `ChimerPub_dump` VALUES ('10029', 'PAX3_FKHR', '', 'PAX3', 'FKHR', '9721857', '-2', 'rhabdomyosarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'These findings indicate that MET, which encodes a receptor involved in growth and motility signaling, is a downstream target of PAX3-FKHR in alveolar rhabdomyosarcoma..     ///    We hypothesize that PAX3-FKHR regulates downstream effector genes involved in rhabdomyosarcoma tumorigenesis.     ///    \"We demonstrate that the expression of MET, but not neural cell adhesion molecule, correlates significantly with PAX3-FKHR expression. \"    ///    We used a myogenic tumor cell culture system and rhabdomyosarcoma tumor specimens to assess candidate gene expression in relationship to various PAX3-FKHR expression levels.     ///    \" The 2;13 chromosomal translocation in alveolar rhabdomyosarcoma generates the chimeric protein PAX3-FKHR, which is a powerful transcriptional activator. \"    ///    Up-regulation of MET but not neural cell adhesion molecule expression by the PAX3-FKHR fusion protein in alveolar rhabdomyosarcoma.. '), ('10030', 'NPM_ALK', '', 'NPM', 'ALK', '16900211', '-2', 'anaplastic large cell lymphoma;non Hodgkin Lymphoma', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'The crucial role of NPM-ALK in the regulation of serpin A1 expression was further demonstrated by using both ectopic expression and downregulation, by RNA interference, of the NPM-ALK oncogene. '), ('10031', 'SYT_SSX1', '', 'SYT', 'SSX1', '11368913', '-2', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'In the present investigation we cloned and sequenced the full-length cDNA of SYT/SSX1, SYT/SSX2 and SYT/SSX4 from synovial sarcoma tissues. '), ('10032', 'TLS_CHOP', 't(12;16)  / ', 'TLS', 'CHOP', '12168660', '-2', 'liposarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'RNA splicing mediated by YB-1 is inhibited by TLS/CHOP in human myxoid liposarcoma cells..     ///    The liposarcoma fusion protein TLS/CHOP retains the ability to bind RNA Pol II but lacks the ability to recruit YB-1 due to replacement of the C-terminal domain of TLS by CHOP.     ///    The oncogenic TLS/CHOP fusion protein inhibits this splicing function of YB-1 in a dominant negative manner. '), ('10033', 'E2A_PBX1', '', 'E2A', 'PBX1', '10637514', '-2', 'acute myeloid leukemia;acute lymphoblastic leukemia;myeloid leukemia;\r\r', '', '', '', '', '', 'Transcription_Factor', '', '', 'Retention of myeloid immortalization by E2a-Pbx1 proteins lacking all Pbx1 sequences N- or C-terminal to the HD indicates that Hox proteins, or a yet undefined factor that binds the Pbx1 HD and derepresses DNA-binding by the HD, cooperate with E2a-Pbx1 in myeloid immortalization..    ///    \"An inhibitory switch derepressed by pbx, hox, and Meis/Prep1 partners regulates DNA-binding by pbx1 and E2a-pbx1 and is dispensable for myeloid immortalization by E2a-pbx1.\"    ///    \"While stabilizing the heterodimer, the 310 helix C-terminal to the Pbx1 HD was also dispensable for the ability of E2a-Pbx1 to heterodimerize with Hox proteins and immortalize myeloblasts.\"'), ('10034', 'SET_CAN', '', 'SET', 'CAN', '8294483', '-2', 'acute myeloid leukemia', '', '', '', '', '', '', '', '', 'Although the function(s) of SET and SET-CAN is not known, we propose that SET plays a key role in the mechanism of leukemogenesis in acute undifferentiated leukemia, perhaps by activating CAN in nuclei and stimulating the transformation potential of SET-CAN. '), ('10035', 'NPM_ALK', 't(2;5)(p23;q35) / ', 'NPM', 'ALK', '9021682', '-2', 'anaplastic large cell lymphoma;non Hodgkin lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'Subsequent cDNA cloning showed p80 to be a fusion protein of two genes, the novel tyrosine kinase gene and the nucleophosmin gene, in accordance with the sequence of the NPM/ALK gene. '), ('10036', 'TLS_ERG', '', 'TLS', 'ERG', '17875932', '-2', 'myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'A related fusion, TLS/ERG, has been found in myeloid leukemia.'), ('10037', 'ETO _AML1', '', 'ETO ', 'AML1', '17058450', '-2', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'Comparative proteomic analysis of human leukemic cells with and without inducible expression of leukemogenic AML1-ETO protein..     ///     AML1-ETO is a leukemogenic fusion protein generated by chromosomal translocation t(8.     ///    The further investigation on their roles in leukemic cells will uncover new clues to understanding leukemogenic effects of AML1-ETO fusion protein.. '), ('10038', 'NPM_ALK', 't(2;5)(p23;q35) / t(2;5) / ', 'NPM', 'ALK', '9209450', '-2', 'anaplastic large cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'Subsequent cDNA cloning revealed p80 to be a fusion protein of two genes, the novel tyrosine kinase gene and the nucleophosmin gene, in accordance with the sequence of the NPM/ALK gene (Morris et al.).     ///    \"Subsequent cDNA cloning showed p80 to be a fusion protein of two genes, the novel tyrosine kinase gene and the nucleophosmin gene, in accordance with the sequence of the NPM/ALK gene (Morris et al, Science 263:1281, 1994). \"'), ('10039', 'SYT_SSX2', '', 'SYT', 'SSX2', '11368913', '-2', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'In the present investigation we cloned and sequenced the full-length cDNA of SYT/SSX1, SYT/SSX2 and SYT/SSX4 from synovial sarcoma tissues.     ///    The SYT/SSX4 and SYT/SSX2 open reading frame also differed from previously reported SYT/SSX sequences by an in-frame addition of 93bp exon located in the junction between exon 7 and 8 of the SYT. '), ('10040', 'FLI1_EWS', '', 'FLI1', 'EWS', '8516324', '-2', 'ewing sarcoma;neuroectodermal tumor;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Deletion of either the EWS domain or the FLI1 corresponding to the DNA-binding domain totally abrogated the ability for EWS-FLI1 to transform 3T3 cells. '), ('10041', 'SYT_SSX2', '', 'SYT', 'SSX2', '16247461', '-2', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'SYT-SSX2, a fusion also frequently found in synovial sarcoma, is necessary for maintaining Igf2 expression in the synovial sarcoma cell line, and the increased IGF2 synthesis protects cells from anoikis and is required for tumor formation in vivo. '), ('10042', 'FUS_ERG', 't(16;21)(p11;q22) / t(16;21)  / ', 'FUS', 'ERG', '10354136', '-3', '', 'PCR;RT-PCR', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', 'Seq', 'The FUS/ERG fusion mRNA was demonstrated in all cases by reverse transcriptase-polymerase chain reaction (RT-PCR).     ///    The relationship between the unique cellular characteristics (especially CD56 and IL-2Ralpha expression) and FUS/ERG protein remains undetermined.. '), ('10043', 'TMPRSS2_ETV1', '', 'TMPRSS2', 'ETV1', '17671502', '-3', 'prostate cancer\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'Whereas TMPRSS2-ERG fusions are predominant, fewer TMPRSS2-ETV1 cases have been identified than expected on the basis of the frequency of high (outlier) expression of ETV1 (refs 3-13). '), ('10044', 'NPM_ALK', '', 'NPM', 'ALK', '7656205', '-3', 'anaplastic large cell lymphoma;non Hodgkin lymphoma;lymphoma\r\r', 'PCR;RT-PCR', 'Kinase', 'Oncogene', '', '', '', '', '', 'In contrast, expression of a NPM/ALK chimeric gene was observed which was absent in the ET. '), ('10045', 'EML4_ALK', '', 'EML4', 'ALK', '24913807', '-3', 'mucinous carcinoma;non small cell lung cancer', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Using the direct RNA sequencing method, we discovered a rare CD74-NRG1 fusion (8 %), an echinoderm microtubule-associated protein like 4 (EML4)-ALK fusion (17 %), and three KRAS mutations (25 %). '), ('10046', 'DMD_BMD', '', 'DMD', 'BMD', '16891620', '-4', 'Duchenne and Becker muscular dystrophy\r\r', '', '', '', '', '', '', '', '', 'Mapping of breakpoints in 26 BMD/DMD patients indicated that the frequency of breakpoint occurrence around this region is 3-fold higher than expected by chance. '), ('10047', 'EWSR1_WT1', '', 'EWSR1', 'WT1', '24395394', '-4', 'brachial plexopathy;peripheral nerve tumor', '', '', '', '', '', '', 'KB', 'Seq', 'A pathognomonic fusion of Ewing sarcoma breakpoint region 1 and Wilms tumor 1 genes (EWSR1/WT1) was present.    ///    A pathognomonic fusion of Ewing sarcoma breakpoint region 1 and Wilms tumor 1 genes (EWSR1/WT1) was present. '), ('10048', 'PBX1_E2A', 't(1;19) / t(1;19)  / ', 'PBX1', 'E2A', '8327485', '-4', 'leukemia\r\r', '', '', '', '', '', 'Transcription_Factor', '', '', 'We further show that promoters containing Pbx1-binding sites are activated by the chimeric E2A-Pbx1 protein but not by Pbx1. '), ('10049', 'MECT1_MAML2', '', 'MECT1', 'MAML2', '23233027', '-4', 'mucoepidermoid carcinoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'MECT1-MAML2 fusion transcripts were demonstrated in 23/37 (62%) MEC.    ///    A subset of MEC were also studied for MECT1-MAML2 fusion transcripts by nested RT-PCR and amplicon sequencing.'), ('10050', 'SYT_SSX2', 'p13;q25 / ', 'SYT', 'SSX2', '11422798', '-4', 'synovial sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Primary synovial sarcoma of the kidney: Report of a case confirmed by molecular detection of the SYT-SSX2 fusion transcripts..     ///    \"The SYT-SSX2 fusion transcripts were detected by a reverse transcription-polymerase chain reaction (RT-PCR) using RNA extracted from formalin-fixed, paraffin-embedded tissue. \"'), ('10051', 'TMPRSS2_ERG', '', 'TMPRSS2', 'ERG', '19401683', '-5', 'prostate cancer\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'As a proof-of-concept, we show the presence of two known prostate cancer biomarkers, PCA-3 and TMPRSS2:ERG the in exosomes isolated from urine of patients, showing the potential for diagnosis and monitoring cancer patients status.. '), ('10052', 'PAX3_FOXO1', '', 'PAX3', 'FOXO1', '21882254', '-5', 'rhabdomyosarcoma;sarcoma\r\r', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', 'KB', 'Seq', 'PAX3-FOXO1 and FGFR4 in alveolar rhabdomyosarcoma.    ///    PAX3-FOXO1 and FGFR4 in alveolar rhabdomyosarcoma..     ///    \"However, we demonstrate that enhanced expression of FGFR4 does not contribute to inhibited differentiation, enhanced proliferation, or transformation downstream of PAX3-FOXO1 in primary mouse myoblasts. \"    ///    \"We hypothesized fibroblast growth factor receptor 4 (FGFR4) may act as an effector of PAX3-FOXO1, contributing to PAX3-FOXO1 tumorigenic phenotypes. \"    ///    Therefore we were unable to identify any contribution of up regulation of wild type FGFR4 to PAX3-FOXO1 driven tumorigenesis.     ///    \" We and others have identified FGFR4 as a direct transcriptional target of the alveolar rhabdomyosarcoma (ARMS) specific fusion protein, PAX3-FOXO1. \"'), ('10053', 'PAX3_FOXO1', '', 'PAX3', 'FOXO1', '25398439', '-5', 'alveolar rhabdomyosarcoma', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', 'KB', 'Seq', 'PLK1 phosphorylates PAX3-FOXO1, the inhibition of which triggers regression of alveolar Rhabdomyosarcoma..     ///    \"Mechanistically, PLK1 interacted with and phosphorylated PAX3-FOXO1 at the novel site S503, leading to protein stabilization. \"    ///    \"Notably, PLK1 inhibition led to elevated ubiquitination and rapid proteasomal degradation of the PAX3-FOXO1 chimeric oncoprotein.\"    ///    \"Notably, PLK1 inhibition led to elevated ubiquitination and rapid proteasomal degradation of the PAX3-FOXO1 chimeric oncoprotein. \"'), ('10054', 'PAX3_FOXO1', '', 'PAX3', 'FOXO1', '24213577', '-5', 'rhabdomyosarcoma;sarcoma\r\r', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', 'KB', 'Seq', 'Transcriptional derepression of F-box protein 32 (FBXO32) (Atrogin1/MAFbx), a gene associated with muscle homeostasis, was evidenced in PAX3-FOXO1 RMS cells silenced for EZH2.    ///    They also suggest that the reducing activity of EZH2 could represent a novel adjuvant strategy to eradicate high-risk PAX3-FOXO1 alveolar RMS.     ///    \"Transcriptional derepression of F-box protein 32 (FBXO32) (Atrogin1/MAFbx), a gene associated with muscle homeostasis, was evidenced in PAX3-FOXO1 RMS cells silenced for EZH2. \"    ///    \"However, the role of EZH2 in the clinically aggressive subgroup of alveolar RMS, characterized by the expression of PAX3-FOXO1 oncoprotein, remains unknown. \"    ///    \"Collectively, these results indicate that EZH2 is a key factor in the proliferation and survival of PAX3-FOXO1 alveolar RMS cells working, at least in part, by repressing FBXO32. \"    ///    The Polycomb group (PcG) protein EZH2 supports the survival of PAX3-FOXO1 alveolar rhabdomyosarcoma by repressing FBXO32 (Atrogin1/MAFbx)..     ///    \"Simultaneous knockdown of FBXO32 and EZH2 in PAX3-FOXO1 RMS cells impaired the pro-apoptotic response, whereas the overexpression of FBXO32 facilitated programmed cell death in EZH2-depleted cells. \"'), ('10055', 'FUS_DDIT3', '', 'FUS', 'DDIT3', '26595521', '-5', 'liposarcoma;sarcoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', 'Seq', 'The receptor tyrosine kinase (RTK) encoding RET was previously identified as a putative downstream target gene to FUS-DDIT3 and here we show that cultured MLS cells expressed phosphorylated RET together with its ligand Persephin.'), ('10056', 'TMPRSS2_ERG', '', 'TMPRSS2', 'ERG', '19664128', '-5', 'prostate cancer\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'Urine fractions from 55 patients (with and without prior prostatic massage) were analyzed for the presence of TMPRSS2:ERG isoforms using real-time qPCR.     ///    \"Sixty-nine percent of urine samples following prostatic massage were positive for TMPRSS2:ERG isoforms a or b, five out of which were positive for both, vs 24% of samples obtained without prior massage. \"    ///    Our findings contribute to the increasing elucidation of the role of TMPRSS2:ERG in the development of prostate cancer.. '), ('10057', 'FUS_DDIT3', '', 'FUS', 'DDIT3', '20017906', '-5', 'liposarcoma;sarcoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', 'Seq', 'In addition, CDK2 showed an increased affinity for cytoskeletal proteins in cells expressing FUS-DDIT3 and DDIT3.    ///    We found that FUS-DDIT3 and the normal DDIT3 bind CDK2.    ///    \"In addition, CDK2 showed an increased affinity for cytoskeletal proteins in cells expressing FUS-DDIT3 and DDIT3. \"    ///    \"In the present study, we searched for putative interaction partners of DDIT3 and the oncogenic FUS-DDIT3 among G1 cyclins and cyclin-dependent kinases. \"    ///    DDIT3 is found as a part of the fusion oncogene FUS-DDIT3 that is causal for the development of myxoid/round-cell liposarcomas (MLS/RCLS).     ///    DDIT3/CHOP and the sarcoma fusion oncoprotein FUS-DDIT3/TLS-CHOP bind cyclin-dependent kinase 2.. '), ('10058', 'TPM3_ALK', '', 'TPM3', 'ALK', '19545284', '-5', 'anaplastic large cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The remaining seven ALCL stained for ALK in the cytoplasm only: two expressed TPM3-ALK, one ATIC-ALK, one MYH9-ALK. '), ('10059', 'MSN_ALK', 't(2;5)(p23;q35) / ', 'MSN', 'ALK', '15297972', '-5', 'anaplastic large cell lymphoma', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Heterogeneity of genomic breakpoints in MSN-ALK translocations in anaplastic large cell lymphoma.. '), ('10060', 'EWSR1_FLI1', '', 'EWSR1', 'FLI1', '19417137', '-5', 'ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'Because these mitotic abnormalities mimic those observed with the knockdown of EWSR1 in zebrafish embryos and HeLa cells, we investigated whether EWSR1/FLI1 interacts with EWSR1 and interferes with its function.    ///    \"Because these mitotic abnormalities mimic those observed with the knockdown of EWSR1 in zebrafish embryos and HeLa cells, we investigated whether EWSR1/FLI1 interacts with EWSR1 and interferes with its function. \"    ///    We show that injection of human or zebrafish EWSR1/FLI1 mRNA into developing zebrafish embryos leads to mitotic defects with multipolar and disorganized mitotic spindles.     ///    This interaction between EWSR1/FLI1 and EWSR1 in Ewing sarcoma may induce mitotic defects leading to genomic instability and subsequent malignant transformation..     ///    \"EWSR1 coimmunoprecipitates with EWSR1/FLI1, and overexpression of EWSR1 rescues the mitotic defects in EWSR1/FLI1-transfected HeLa cells. \"    ///    Ewing sarcoma fusion protein EWSR1/FLI1 interacts with EWSR1 leading to mitotic defects in zebrafish embryos and human cell lines.. '), ('10061', 'RET_KIF5B', '', 'RET', 'KIF5B', '22327624', '-5', 'adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'KIF5B-RET fusions in lung adenocarcinoma..     ///    \"The KIF5B-RET fusion leads to aberrant activation of RET kinase and is considered to be a new driver mutation of LADC because it segregates from mutations or fusions in EGFR, KRAS, HER2 and ALK, and a RET tyrosine kinase inhibitor, vandetanib, suppresses the fusion-induced anchorage-independent growth activity of NIH3T3 cells.. \"'), ('10062', 'NUP98_ADD3', 't(10;11)(q25;p15) / t(4;11)(q21;p15) / ', 'NUP98', 'ADD3', '12810632', '-6', 'T ALL;leukemia\r\r', '', '', '', '', '', '', 'KB', '', 'Both NUP98-ADD3 and ADD3-NUP98 fusion transcripts are expressed in the patient. '), ('10063', 'RARA_PML', '', 'RARA', 'PML', '8161469', '-6', 'acute promyelocytic leukemia;leukemia\r\r', '', '', 'Oncogene', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'This results in a PML-RARA chimeric gene. '), ('10064', 'EWSR1_FLI1', '', 'EWSR1', 'FLI1', '19528446', '-7', '', '', '', '', '', '', '', 'KB', 'Seq', 'Synthetic RNAs corresponding to EWSR1-FLI1 were used as substrates.    ///    Cleavage of the Ewing tumour-specific EWSR1-FLI1 mRNA by hammerhead ribozymes..     ///    \"Therefore, inactivation of EWSR1-FLI1 is an interesting strategy for EFT therapy. \"    ///    The RNA corresponding to EWSR1-FLI1 is accessible for ribozyme mediated inactivation and ribozymes are able to cleave EWSR1-FLI1 specific RNA in the presence of a high background of normal cellular RNAs..     ///    A ribozyme with specificity for EWSR1-FLI1 was developed and the activity in vitro was investigated.     ///    \"In the majority of EFT, EWSR1-FLI1 (Ewing sarcoma breakpoint region 1-Friend leukaemia virus integration 1) fusion proteins can be detected and EWSR1-FLI1 substantially contributes to the malignant phenotype of EFT.\"    ///    \"In the majority of EFT, EWSR1-FLI1 (Ewing sarcoma breakpoint region 1-Friend leukaemia virus integration 1) fusion proteins can be detected and EWSR1-FLI1 substantially contributes to the malignant phenotype of EFT. \"'), ('10065', 'FLI1_EWSR1', 't(14;22)(q32;q12) / ', 'FLI1', 'EWSR1', '23630070', '-7', 'mesothelioma', '', '', '', '', '', '', '', 'Seq', 'The EWSR1 breakpoint in exon 8 in the EWSR1-YY1 chimeric transcript is similar to what is found in other fusions involving EWSR1 such as EWSR1-FLI1, EWSR1-DDIT3, and EWSR1-ATF1.     ///    \"The EWSR1 breakpoint in exon 8 in the EWSR1-YY1 chimeric transcript is similar to what is found in other fusions involving EWSR1 such as EWSR1-FLI1, EWSR1-DDIT3, and EWSR1-ATF1.\"'), ('10066', 'EWSR1_ATF1', 't(14;22)(q32;q12) / ', 'EWSR1', 'ATF1', '23630070', '-7', 'mesothelioma', '', '', '', '', '', 'Transcription_Factor', 'KB', 'Seq', 'The EWSR1 breakpoint in exon 8 in the EWSR1-YY1 chimeric transcript is similar to what is found in other fusions involving EWSR1 such as EWSR1-FLI1, EWSR1-DDIT3, and EWSR1-ATF1. '), ('10067', 'PPARG_PAX8', '', 'PPARG', 'PAX8', '20564403', '-7', 'neuroblastoma\r\r', '', '', '', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'Chromosomal RET-PTC and PAX8-PPARgamma rearrangements were observed in 20% and 17% of tumors, respectively.     ///    RET-PTC and PAX8-PPARgamma rearrangements and mutations of the neuroblastoma RAS viral oncogene homolog N-RAS at codon 61 were the most common genetic alterations in FVPTCs.     ///    \"Tumors and matched normal thyroid samples were tested for RAS, for the v-raf murine sarcoma viral oncogene (BRAF) substitution of valine (V) for glutamate (E) at codon 600 (the V600E mutation), for phosphatase and tensin homolog (PTEN), for catalytic PI3k p110 subunit alpha (PIK3CA), for AKT, and for the presence of rearranged during transfection (ret) proto-oncogene/PTC (RET-PTC) and paired box-8 (PAX8)/peroxisome proliferator-activated receptor gamma (PPARgamma) fusion protein (PAX8-PPARgamma) rearrangements by direct sequencing and reverse transcriptase-polymerases chain reaction analyses, respectively. \"'), ('10068', 'EWSR1_DDIT3', 't(14;22)(q32;q12) / ', 'EWSR1', 'DDIT3', '23630070', '-7', 'mesothelioma', '', '', '', '', '', 'Transcription_Factor', 'KB', '', 'The EWSR1 breakpoint in exon 8 in the EWSR1-YY1 chimeric transcript is similar to what is found in other fusions involving EWSR1 such as EWSR1-FLI1, EWSR1-DDIT3, and EWSR1-ATF1. '), ('10069', 'MK2_EGF', '', 'MK2', 'EGF', '17110203', '-8', '', '', '', '', '', '', '', '', '', 'The MK2-EGF translocation response is susceptible to other classes of inhibitors, including nonselective kinase inhibitors, kinase inhibitors that inhibit upstream kinases in the p38 MAPK signaling pathway, and kinases involved in cross talk between different modules (ERKs, JNKs, and p38s) of the MAPK signaling pathways. '), ('10070', 'PAX3_FOXO1', '', 'PAX3', 'FOXO1', '23645752', '-8', 'rhabdomyosarcoma;neuroblastoma;sarcoma\r\r', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', 'KB', 'Seq', ' The majority of alveolar rhabdomyosarcoma (ARMS) are distinguished through the paired box 3-forkhead box protein O1 (PAX3-FOXO1) fusion oncoprotein, being generated by a 2;13 chromosomal translocation.     ///    \"Pulse-chase and cycloheximide experiments suggest that GREM1, DAPK1, and MYOD1 are directly regulated by PAX3-FOXO1.\"    ///    PAX3-FOXO1 appears to indirectly down-regulate HEY1 by up-regulating MYCN.    ///    Data reveal that the growth-suppressive activity of high PAX3-FOXO1 expression is closely-associated with up-regulation of the GREM1 and DAPK1 tumor-suppressor genes.     ///    \"The present study characterized four genes [gremlin 1 (GREM1), death-associated protein kinase-1 (DAPK1), myogenic differentiation-1 (MYOD1), and hairy/enhancer-of-split related with YRPW motif-1 (HEY1)] as targets of PAX3-FOXO1. \"    ///    The roles of PAX3-FOXO1 and MYCN expression were examined.     ///    This study characterized four downstream targets of PAX3-FOXO1 that contribute to the biological activities of growth suppression and myogenic differentiation..     ///    \"Pulse-chase and cycloheximide experiments suggest that GREM1, DAPK1, and MYOD1 are directly regulated by PAX3-FOXO1. \"    ///    Regulation of target genes of PAX3-FOXO1 in alveolar rhabdomyosarcoma..     ///    \"The expression of the four genes, PAX3-FOXO1, and v-myc myelocytomatosis viral-related oncogene, neuroblastoma-derived (avian) (MYCN) was determined in various ARMS cell models and primary tumors. \"'), ('10071', 'E2A_PBX1', '', 'E2A', 'PBX1', '10454582', '-8', 'leukemia\r\r', '', '', '', '', '', 'Transcription_Factor', '', '', 'A recurrent translocation between chromosome 1 (Pbx1) and 19 (E2A) leading to the expression of the E2A-Pbx1 fusion oncoprotein occurs in approximately 5 to 10% of acute leukemias in humans.    ///     A recurrent translocation between chromosome 1 (Pbx1) and 19 (E2A) leading to the expression of the E2A-Pbx1 fusion oncoprotein occurs in approximately 5 to 10% of acute leukemias in humans. '), ('10072', 'TLS_ERG', '', 'TLS', 'ERG', '9653171', '-8', 'myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'Thus, TLS-ERG expression alone induced a leukemogenic program that exhibited similarities to the human disease associated with this translocation.     ///    \"Here, we report that retroviral transduction of TLS-ERG, a myeloid leukemia-associated fusion gene, to human cord blood cells results in altered myeloid and arrested erythroid differentiation and a dramatic increase in the proliferative and self-renewal capacity of transduced myeloid progenitors. \"    ///    Retroviral transduction of TLS-ERG initiates a leukemogenic program in normal human hematopoietic cells.. '), ('10073', 'NPM_ALK', 't(2;5)(p23;q35) / t(2;5)  / ', 'NPM', 'ALK', '15883821', '-8', 'anaplastic large cell lymphoma;hematopoietic malignancy;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'NPM-ALK activates the antiapoptotic phosphatidylinositol-3 kinase/Akt (PI3K/Akt) signaling pathway, which plays a critical role in cell survival and apoptosis. '), ('10074', 'TMPRSS2_ERG', '', 'TMPRSS2', 'ERG', '21167530', '-9', 'prostate cancer\r\r', '', '', '', '', '', '', 'KB', 'Seq', ' We evaluated the clinicopathological characteristics of single focus prostate cancer in radical prostatectomies, its clinical relevance and the occurrence of TMPRSS2-ERG rearrangement. '), ('10075', 'SLC45A3_ELK4', '', 'SLC45A3', 'ELK4', '22787087', '-9', 'prostate cancer\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'Using a series of detailed experiments, Zhang and colleagues establish that the prostate cancer RNA chimera SLC45A3-ELK4 is generated by cis-splicing between the 2 adjacent genes and does not involve DNA rearrangements or trans-splicing.    ///    \" Using a series of detailed experiments, Zhang and colleagues establish that the prostate cancer RNA chimera SLC45A3-ELK4 is generated by cis-splicing between the 2 adjacent genes and does not involve DNA rearrangements or trans-splicing. \"    ///    SLC45A3-ELK4 chimera in prostate cancer: spotlight on cis-splicing.. '), ('10076', 'BCR_ABL1', '', 'BCR', 'ABL1', '19157547', '-9', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia\r\r', 'PCR;RT-PCR', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'However, BCR-ABL1 expression may not reflect the percentage of leukemic cells as FCM and IG/TCR rearrangement quantification do, and these methods are thus complementary..     ///    The other discordant case showed high BCR-ABL1 RNA level while the other methods did not detect any MRD. '), ('10077', 'EML4_ALK', '', 'EML4', 'ALK', '25806325', '-10', 'anaplastic large cell lymphoma;non small cell lung cancer;lung cancer;ly\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'In the last five years the interest for ALK small inhibitors grew rapidly, mainly because it was discovered that a small but significant percentage of non-small cell lung cancer (NSCLC) patients carries the oncogenic fusion protein EML4-ALK, in addition to about half percent of anaplastic large cell lymphoma (ALCL) patients, an aggressive but definitely rarer non Hodgkin\'s T cell lymphoma, and other malignancies.    ///    \"In the last five years the interest for ALK small inhibitors grew rapidly, mainly because it was discovered that a small but significant percentage of non-small cell lung cancer (NSCLC) patients carries the oncogenic fusion protein EML4-ALK, in addition to about half percent of anaplastic large cell lymphoma (ALCL) patients, an aggressive but definitely rarer non Hodgkin\'s T cell lymphoma, and other malignancies. \"'), ('10078', 'PPARG_PAX8', '', 'PPARG', 'PAX8', '12364466', '-10', 'colon cancer', '', '', '', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'PPAR gamma gene mutations have been found in 4 of 55 sporadic colon cancers, and a chimeric PAX8-PPAR gamma 1 gene frequently generates a chromosomal translocation in thyroid follicular carcinomas, implicating PPAR gamma in tumor suppression. '), ('10079', 'TPM3_ALK', '', 'TPM3', 'ALK', '17660712', '-10', 'anaplastic large cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Overexpression and activation of TPM3-ALK tyrosine kinase fusion protein is a causal oncogenic event in the development of Anaplastic Large Cell Lymphoma and Inflammatory Myofibroblastic ALK-positive tumors.'), ('10080', 'SSX_SS18', '', 'SSX', 'SS18', '17018603', '-11', 'synovial sarcoma', '', '', '', '', '', '', '', '', 'The domains involved in these opposite transcriptional activities are retained in the SS18-SSX fusion proteins. '), ('10081', 'MLL_ENL', '', 'MLL', 'ENL', '19144982', '-11', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Patient samples were investigated by RT-PCR for MLL-AF4, MLL-ENL, and MLL-AF9 and by long-distance inverse polymerase chain reaction, thus also allowing the identification of unknown MLL fusion partners at the genomic level.     ///    MLL-AF4 was detected in 101 (54.9%) and MLL-ENL in 11 (6.0%) cases. '), ('10082', 'SRY_NLS', '', 'SRY', 'NLS', '16762365', '-11', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'In a male embryonic gonadal cell line, M64I and M64A SRY-NLS fusion proteins exhibit native transcriptional activation of Sox9, a key step in testicular differentiation. '), ('10083', 'SSX_SS18', '', 'SSX', 'SS18', '17117414', '-11', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Since the domains involved in these apparently opposite transcription regulatory activities are retained in the SS18-SSX fusion proteins, we hypothesize that these fusion proteins function as \"activator-repressors\" of transcription. '), ('10084', 'SYT_SSX2', '', 'SYT', 'SSX2', '15500711', '-13', 'leiomyosarcoma', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Of the 34 cases of SS 28 (93.3%) expressed SSX-SYT chimeric transcripts (14 were positive for SYT-SSX1, 9 for SYT-SSX2). '), ('10085', 'EML4_ALK', '', 'EML4', 'ALK', '22690483', '-13', 'breast cancer;lung cancer;melanoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Examples are imatinib in CML and GIST, trastuzumab in HER2 positive breast cancer, gefitinib in mutated EGFR, crizotinib in EML4-ALK positive lung cancer and, also, vemurafenib in BRAF 600E mutated metastatic melanoma.    ///    \"Examples are imatinib in CML and GIST, trastuzumab in HER2 positive breast cancer, gefitinib in mutated EGFR, crizotinib in EML4-ALK positive lung cancer and, also, vemurafenib in BRAF 600E mutated metastatic melanoma. \"'), ('10086', 'HNRPA2B1_ETV1', '', 'HNRPA2B1', 'ETV1', '20693979', '-13', 'prostate cancer\r\r', 'RT-PCR', '', '', '', '', '', '', '', 'We identified 54 TMPRSS2:ERG-positive cases (54/194, 28%) and two HNRPA2B1:ETV1-positive cases (2/194, 1%). '), ('10087', 'SYT_SSX1', '', 'SYT', 'SSX1', '15500711', '-13', 'leiomyosarcoma', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Of the 34 cases of SS 28 (93.3%) expressed SSX-SYT chimeric transcripts (14 were positive for SYT-SSX1, 9 for SYT-SSX2). '), ('10088', 'PSF_TFE3', '', 'PSF', 'TFE3', '19563413', '-13', 'renal cell carcinoma\r\r', '', '', '', '', '', '', '', '', 'The smooth muscle stroma was positive for alpha-smooth muscle actin and h-caldesmon, but reverse transcription-polymerase chain reaction of the tumor using frozen material could not detect any previously reported chimeric transcripts including ASPL-TFE3, PRCC-TFE3, CLTC-TFE3, PSF-TFE3 or NoNo-TFE3.    ///    \"The smooth muscle stroma was positive for alpha-smooth muscle actin and h-caldesmon, but reverse transcription-polymerase chain reaction of the tumor using frozen material could not detect any previously reported chimeric transcripts including ASPL-TFE3, PRCC-TFE3, CLTC-TFE3, PSF-TFE3 or NoNo-TFE3. \"'), ('10089', 'TMPRSS2_ERG', '', 'TMPRSS2', 'ERG', '25779129', '-14', 'prostate cancer\r\r', 'PCR', '', '', '', '', '', 'KB', 'Seq', 'On the other hand, qRT-PCR exhibited a higher sensitivity, as TMPRSS2-ERG transcripts were detected in as few as 100 VCaP cells, in comparison to NanoString methodologies which detected ERG from 10,000 cells.    ///    \"On the other hand, qRT-PCR exhibited a higher sensitivity, as TMPRSS2-ERG transcripts were detected in as few as 100 VCaP cells, in comparison to NanoString methodologies which detected ERG from 10,000 cells. \"    ///    \"We utilized TMPRSS2-ERG positive VCaP and TMPRSS2-ERG negative LNCaP cells to simulate three different sample types (cells, tissue, and post-DRE urine sediment). \"'), ('10090', 'SYT_SSX2', '', 'SYT', 'SSX2', '15641030', '-14', 'synovial sarcoma;sarcoma\r\r', 'PCR', '', '', '', '', '', '', '', 'SYT/SSX1 translocations are seen in nearly three times as many synovial sarcomas as SYT/SSX2 translocations.     ///    \"Although the SYT/SSX2 fusion is usually associated with the monophasic disease pattern, the SYT/SSX1 fusion is present in tumors with biphasic or monophasic patterns. \"'), ('10091', 'EML4_ALK', '', 'EML4', 'ALK', '19383809', '-14', 'lung cancer\r\r', 'PCR', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Immunohistochemical detection of EML4-ALK has proved difficult, however, likely as a result of low transcriptional activity conferred by the promoter-enhancer region of EML4.     ///    Our iAEP method discriminated between tumors positive or negative for EML4-ALK in a test set of specimens.     ///    The sensitivity of EML4-ALK detection by immunohistochemistry should be increased adequately.     ///    \"These 8 tumors were found to include 1 with EML4-ALK variant 1, 1 with variant 2, 3 with variant 3, and 2 with previously unidentified variants (designated variants 6 and 7). \"    ///    \" EML4-ALK is a transforming fusion tyrosine kinase, several isoforms of which have been identified in lung cancer. \"'), ('10092', 'RET_PTC3', '', 'RET', 'PTC3', '11747322', '-14', 'lymphocytic thyroiditis', 'PCR;RT-PCR', 'Kinase', 'Oncogene', '', '', '', '', '', 'Furthermore, using a polyclonal ret antibody, an apical or a diffuse cytoplasmic ret onc protein immunolabelling was observed in the three patients with RET/PTC1 rearrangement and in the three patients with RET/PTC3 rearrangement. '), ('10093', 'NUP98_HOXA9', '', 'NUP98', 'HOXA9', '15454493', '-15', 'myeloid leukemia;leukemia\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', 'KB', 'Seq', 'Identification of cooperative genes for NUP98-HOXA9 in myeloid leukemogenesis using a mouse model..     ///    These genes cooperated with NUP98-HOXA9 in transforming NIH 3T3 cells.     ///    \"This suggested that the NUP98-HOXA9 fusion induced a preleukemic phase, and other factors were required for complete leukemogenesis. \"    ///    We generated a transgenic mouse line that specifically expressed the chimeric NUP98-HOXA9 gene in the myeloid lineage.     ///    NUP98-HOXA9 expression promoted the onset of retrovirus-induced BXH2 myeloid leukemia. '), ('10094', 'ATIC_ALK', '', 'ATIC', 'ALK', '10706082', '-15', 'anaplastic large cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', '', 'Expression of full-length ATIC-ALK cDNA in mouse fibroblasts revealed that the fusion protein (a) possesses constitutive tyrosine kinase activity; (b) forms stable complexes with the signaling proteins Grb2 and Shc; (c) induces tyrosine-phosphorylation of Shc; and (d) provokes oncogenic transformation.    ///    Nucleotide sequence analysis of ALK transcripts isolated by 5\'-rapid amplification of cDNA ends revealed a chimeric mRNA corresponding to an ATIC-ALK in-frame fusion.'), ('10095', 'E2F1_ESR1', '', 'E2F1', 'ESR1', '17173074', '-15', 'breast cancer\r\r', '', '', '', '', 'Receptor', 'Transcription_Factor', '', '', 'An E2F1-estrogen receptor fusion protein activated the endogenous p57 promoter in response to hydroxytamoxifen treatment in the presence of cycloheximide. '), ('10096', 'P300_MLL', 't(11;22)(q23;q13) / ', 'P300', 'MLL', '9389684', '-15', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'We identify here that the p300 gene is fused to the MLL gene and that in-frame MLL-p300 fusion protein is generated in acute myeloid leukemia (AML) with t(11. '), ('10097', 'NPM_ALK', '', 'NPM', 'ALK', '15184887', '-16', 'anaplastic large cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'It has been shown that NPM-ALK binds to and activates signal transducer and activator of transcription 3 (STAT3) in vitro, and that STAT3 is constitutively active in ALK(+) ALCL cell lines and tumors. '), ('10098', 'ETV6_CBFA2', '', 'ETV6', 'CBFA2', '11675129', '-16', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'To investigate the influence of ETV6/CBFA2 on cellular transformation, the fusion gene was cloned into a murine ecotropic retroviral vector and transduced into IL-3-dependent Ba/F3 and 32Dcl.3 and IL-7-dependent IxN/2b murine hematopoietic cell lines.     ///    We further investigated the effect of ETV6/CBFA2 expression in vivo by generating transgenic mice in which expression of the fusion was directed to lymphoid cells using the immunoglobulin heavy chain enhancer/promoter.     ///    We conclude that the expression of ETV6/CBFA2 alone is not sufficient for induction of growth factor independence in hematopoietic cell lines or hematologic disease in transgenic mice..     ///    \" ETV6/CBFA2 (TEL/AML1) is the most frequent genetic abnormality associated with acute lymphoblastic leukemias in children, and is associated with a favorable prognosis. \"    ///    \"The mice did not develop a malignant hematologic disorder, nor did they display histopathologic, morphologic, or immunophenotypic abnormalities, although ETV6/CBFA2 expression was confirmed in each line. \"    ///    The expression of ETV6/CBFA2 (TEL/AML1) is not sufficient for the transformation of hematopoietic cell lines in vitro or the induction of hematologic disease in vivo..     ///    \"However, although Western blot analysis demonstrated expression of each variant, none of the stable cell lines expressing CBFA2/ETV6 or the variants conferred factor-independent growth. \"    ///    \"Different variants of ETV6/CBFA2, corresponding to CBFA2 alternatively spliced variants, and the reciprocal product CBFA2/ETV6, were stably expressed in each of these cell lines. \"'), ('10099', 'SUZ12_JAZF1', '', 'SUZ12', 'JAZF1', '24530230', '-16', 'endometrial stromal sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', 'KB', '', ' The chimeric transcripts described in endometrial stromal sarcomas (ESS) are JAZF1/SUZ12, YWHAE/FAM22, ZC3H7/BCOR, MBTD1/CXorf67, and recombinations of PHF1 with JAZF1, EPC1, and MEAF6. '), ('10100', 'MBTD1_CXORF67', '', 'MBTD1', 'CXORF67', '24530230', '-16', 'endometrial stromal sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', 'KB', '', ' The chimeric transcripts described in endometrial stromal sarcomas (ESS) are JAZF1/SUZ12, YWHAE/FAM22, ZC3H7/BCOR, MBTD1/CXorf67, and recombinations of PHF1 with JAZF1, EPC1, and MEAF6.     ///    \"The chimeric transcripts described in endometrial stromal sarcomas (ESS) are JAZF1/SUZ12, YWHAE/FAM22, ZC3H7/BCOR, MBTD1/CXorf67, and recombinations of PHF1 with JAZF1, EPC1, and MEAF6.\"'), ('10101', 'TLS_ERG', '', 'TLS', 'ERG', '15988032', '-16', 'ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'To unveil the potential mechanism(s) underlying cellular transformation, we have investigated the effects of TLS-ERG on both gene transcription and RNA splicing.     ///    Microarray analysis of RNA samples from these cells showed that TLS-ERG activates two different sets of genes sharing little similarity in the two cell lines.     ///    Deletion analysis of TLS-ERG in both mouse L-G myeloid progenitor cells and NIH 3T3 fibroblasts revealed that the RNA Pol II-interacting domain of TLS-ERG resides within the first 173 amino acids.     ///    The oncogenic TLS-ERG fusion protein is found in human myeloid leukemia and Ewing\'s sarcoma as a result of specific chromosomal translocation.    ///     The oncogenic TLS-ERG fusion protein is found in human myeloid leukemia and Ewing\'s sarcoma as a result of specific chromosomal translocation.     ///    \"While TLS-ERG repressed expression of the luciferase reporter gene driven by glycoprotein IX promoter in L-G cells but not in NIH 3T3 cells, the fusion protein was able to affect splicing of the E1A reporter in NIH 3T3 cells but not in L-G cells. \"    ///    \"Taken together, these results suggest that the oncogenic TLS-ERG fusion protein transforms hematopoietic cells and fibroblasts via different pathways.. \"    ///    The oncogenic TLS-ERG fusion protein exerts different effects in hematopoietic cells and fibroblasts..     ///    \"To identify potential target genes of TLS-ERG, the fusion protein and its mutants were stably expressed in both L-G and NIH 3T3 cells through retroviral transduction. \"'), ('10102', 'ETV6_NTRK3', '', 'ETV6', 'NTRK3', '15143160', '-17', '', '', 'Kinase', '', '', '', '', 'KB', 'Seq', 'ETV6-NTRK3 (EN), comprised of the ETV6 SAM domain fused to the NTRK3 PTK, is unique among ETV6 chimeric oncoproteins, as it is expressed in cancers of multiple lineages.    ///    \"ETV6-NTRK3 (EN), comprised of the ETV6 SAM domain fused to the NTRK3 PTK, is unique among ETV6 chimeric oncoproteins, as it is expressed in cancers of multiple lineages. \"    ///    Mutations in the SAM domain of the ETV6-NTRK3 chimeric tyrosine kinase block polymerization and transformation activity.. '), ('10103', 'ETV6_NTRK3', '', 'ETV6', 'NTRK3', '16258068', '-17', '', '', 'Kinase', '', '', '', '', 'KB', 'Seq', 'The ETV6-NTRK3 (EN) chimeric tyrosine kinase, a potent oncoprotein expressed in tumors derived from multiple cell lineages, functions as a constitutively active protein tyrosine kinase.    ///    The ETV6-NTRK3 chimeric tyrosine kinase suppresses TGF-beta signaling by inactivating the TGF-beta type II receptor..     ///    \"The ETV6-NTRK3 (EN) chimeric tyrosine kinase, a potent oncoprotein expressed in tumors derived from multiple cell lineages, functions as a constitutively active protein tyrosine kinase. \"'), ('10104', 'EWS_ETV1', '', 'EWS', 'ETV1', '12736494', '-17', 'neuroectodermal tumor;ewing sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Different chimeric genes, EWS-ERG and EWS-ETV1, were detected in the other two ES samples. '), ('10105', 'NPM_ALK', '', 'NPM', 'ALK', '19131793', '-17', 'anaplastic large cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'This finding was confirmed by reverse transcription-polymerase chain reaction analysis of the NPM/ALK fusion protein. '), ('10106', 'EWS_ERG', '', 'EWS', 'ERG', '12736494', '-17', 'neuroectodermal tumor;ewing sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'Different chimeric genes, EWS-ERG and EWS-ETV1, were detected in the other two ES samples. '), ('10107', 'NPM_ALK', '', 'NPM', 'ALK', '18509351', '-18', 'anaplastic large cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'To conclude, for the first time, we demonstrate the importance of the IL-22 autocrine pathway in a lymphoid malignancy, and reveal yet another novel function of NPM-ALK.. '), ('10108', 'SQSTM1_ALK', '', 'SQSTM1', 'ALK', '21134980', '-18', 'B cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'this led to the identification of SQSTM1-ALK.     ///    \"Identification of a novel fusion, SQSTM1-ALK, in ALK-positive large B-cell lymphoma.. \"    ///    \"SQSTM1-ALK may be a rare fusion, but our data provide novel biological insights and serve as a key for the accurate diagnosis of this rare lymphoma.. \"    ///    We showed transforming activities of SQSTM1-ALK with a focus formation assay and an in vivo tumorigenicity assay using 3T3 fibroblasts infected with a recombinant retrovirus encoding SQSTM1-ALK. '), ('10109', 'TORC1_MAML2', '', 'TORC1', 'MAML2', '14536081', '-18', 'mucoepidermoid carcinoma\r\r', '', '', '', '', '', '', '', '', 'As expression of the TORC1-MAML2 chimera strongly induced target gene expression via CREB, our results reveal a mechanism by which CREB stimulates transcription in normal and transformed cells..    ///    \"As expression of the TORC1-MAML2 chimera strongly induced target gene expression via CREB, our results reveal a mechanism by which CREB stimulates transcription in normal and transformed cells.. \"'), ('10110', 'NPM_ALK', '', 'NPM', 'ALK', '21134980', '-18', 'B cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'We examined an ALK-positive large B-cell lymphoma case showing an anti-ALK immunohistochemistry pattern distinct from those of 2 known ALK fusions, CLTC-ALK and NPM-ALK, for the presence of a novel ALK fusion. '), ('10111', 'MLL_EEN', '', 'MLL', 'EEN', '9122235', '-18', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'Sequence analysis of the fusion MLL/EEN transcript in our patient reveals that exon 6 of MLL is fused to the N-terminal end of EEN, a fusion that would create a chimeric protein that includes the major functional domain of EEN. '), ('10112', 'FUS_BBF2H7', '', 'FUS', 'BBF2H7', '15201968', '-18', 'chondrosarcoma;synovial sarcoma;liposarcoma;fibrous histiocytoma;sarcoma;histiocytoma\r\r', '', '', 'Oncogene', '', '', 'Transcription_Factor', '', '', 'Thus, we investigated the expression of DOL54 in low grade fibromyxoid sarcoma (LGFMS) carrying the FUS-BBF2H7 chimeric transcript.     ///    \"DOL54 expression was found in 8/12 LGFMS carrying the FUS-BBF2H7 chimera but also in 8/10 of the examined MFH, 5/7 SS, 2/5 ET and 7/7 examined EMC. \"'), ('10113', 'RET_PTC3', '', 'RET', 'PTC3', '18583418', '-18', '', '', 'Kinase', 'Oncogene', '', '', '', '', '', ' We studied gene expression profiles in two mouse models of human thyroid carcinoma: the Tg-RET/PTC3 (RP3) and Tg-E7 mice.     ///    Gene expression in RET/PTC3 and E7 transgenic mouse thyroids: RET/PTC3 but not E7 tumors are partial and transient models of human papillary thyroid cancers.. '), ('10114', 'EML4_ALK', '', 'EML4', 'ALK', '25971657', '-18', 'lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Constitutive dimerization of EML4-ALK mediated by a dimerization motif of EML4 results in kinase activation.    ///    The EML4-ALK oncogene: targeting an essential growth driver in human cancer.    ///    The EML4-ALK oncogene: targeting an essential growth driver in human cancer..     ///    \"By screening such a library of lung adenocarcinoma with a focus formation assay, we discovered the EML4-ALK fusion-type oncogene. \"'), ('10115', 'CLTC_ALK', '', 'CLTC', 'ALK', '21134980', '-18', 'B cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', '', 'We examined an ALK-positive large B-cell lymphoma case showing an anti-ALK immunohistochemistry pattern distinct from those of 2 known ALK fusions, CLTC-ALK and NPM-ALK, for the presence of a novel ALK fusion. '), ('10116', 'NHE3_CFP', '', 'NHE3', 'CFP', '17303069', '-19', '', '', '', '', '', '', '', '', '', 'Separation of cellular acidification from Na(+) removal revealed that only NHE3-CFP translocated when medium Na(+) was removed, and only NHE2-CFP translocated when the cell was acidified.     ///    \"A protocol commonly used to activate the Na(+)/H(+) exchange function (NH(4)-prepulse acid load sustained in Na(+)-free medium), increased PM percentages of PM NHE3-CFP and NHE2-CFP. \"    ///    NHE2-CFP or NHE3-CFP fusion proteins were functional Na(+)/H(+) exchangers when transiently expressed in NHE-deficient PS120 fibroblasts. '), ('10117', 'IRAP_GLUT4', '', 'IRAP', 'GLUT4', '16967782', '-19', 'diabetes\r\r', '', '', '', '', '', '', '', '', 'In this study we measured the cell surface IRAP activity and 3-O-[methyl-14C]-D-Glucose uptake in adipocytes isolated from Otsuka Long Evans Tokushima Fatty rats (OLETF), developed as a model of type 2 diabetes mellitus, to evaluate whether the translocation of GLUT4/IRAP vesicles is affected.     ///    Continuous measurement of cell surface IRAP activity allowed accurate evaluations of GLUT4/IRAP vesicle translocation and of the establishment of defects in OLETF rats.. '), ('10118', 'CFP_NHE2', '', 'CFP', 'NHE2', '17303069', '-19', '', '', '', '', '', '', '', '', '', 'Separation of cellular acidification from Na(+) removal revealed that only NHE3-CFP translocated when medium Na(+) was removed, and only NHE2-CFP translocated when the cell was acidified.     ///    \"A protocol commonly used to activate the Na(+)/H(+) exchange function (NH(4)-prepulse acid load sustained in Na(+)-free medium), increased PM percentages of PM NHE3-CFP and NHE2-CFP. \"    ///    NHE2-CFP or NHE3-CFP fusion proteins were functional Na(+)/H(+) exchangers when transiently expressed in NHE-deficient PS120 fibroblasts. '), ('10119', 'NPM_ALK', 't(2;5)(p23;q35) / t(2;5)  / ', 'NPM', 'ALK', '9450809', '-19', 'anaplastic large cell lymphoma;non Hodgkin lymphoma;lymphoma\r\r', 'PCR;RT-PCR', 'Kinase', 'Oncogene', '', '', '', '', '', 'This finding was confirmed both by RT-PCR analysis of the NPM/ALK fusion protein and by positive staining with the p80(NPM/ALK) antibody. '), ('10120', 'HDAC1_GAL4', '', 'HDAC1', 'GAL4', '16121030', '-19', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'Gal4-HDAC1 fusion, targeted proximally to the GC-boxes, potently repressed the transcription of pG5-5x(GC)-Luc, in which Sp1 potently activates transcription. '), ('10121', 'EML4_ALK', '', 'EML4', 'ALK', '23415374', '-19', 'adenocarcinoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The EML4-ALK transcript or CHFR hypermethylation was found in 11 (6.7%) or 16 (10%) adenocarcinomas, respectively, whereas EGFR or KRAS mutation was detected in 48 (29%) or 13 (8%) cases, respectively.     ///    \"The EML4-ALK transcript or CHFR hypermethylation was found in 11 (6.7%) or 16 (10%) adenocarcinomas, respectively, whereas EGFR or KRAS mutation was detected in 48 (29%) or 13 (8%) cases, respectively.\"    ///    \" Excluding epidermal growth factor receptor (EGFR) mutation, v-Ki-ras2/Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation, and echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) fusion, the genetic alterations involved in lung adenocarcinogenesis, especially those linked to poor clinical outcomes, are still unknown. \"'), ('10122', 'SSX_SYT', '', 'SSX', 'SYT', '17418413', '-20', 'synovial sarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', ' Synovial sarcoma is an aggressive soft-tissue malignancy marked by a unique t(X;18) translocation leading to expression of a chimeric SYT-SSX fusion protein. '), ('10123', 'MLL_LASP1', 't(11;17)(q23;q21) / ', 'MLL', 'LASP1', '12527918', '-20', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', 'FISH;PCR;RT-PCR ', '', '', '', '', '', 'KB', '', 'Retroviral transduction of myeloid progenitors demonstrated that MLL/LASP1 is the fourth known fusion of MLL with a cytoplasmic protein that has no in vitro transformation capability, thus establishing a potential subgroup among the MLL fusion proteins.. '), ('10124', 'SYT_SSX1', '', 'SYT', 'SSX1', '15045545', '-20', 'synovial sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'SYT-SSX1 chimeric genes could be detected in the samples obtained from up to 3 cm outside the tumor by RT-PCR. '), ('10125', 'PAX3_FKHR', '', 'PAX3', 'FKHR', '7495283', '-21', 'alveolar rhabdomyosarcoma;desmoplastic small round cell tumor;ewing sarcoma;neuroectodermal tumor;rhabdomyosarcoma', '', '', '', '', '', '', '', '', 'To investigate the structure and potential diagnostic utility of the detection of EWS-WT1 chimeric RNA in desmoplastic small round cell tumor, 12 examples of this entity and 49 other tumors that enter in its differential diagnosis were studied by reverse transcriptase polymerase chain reaction for the presence of EWS-WT1, EWS-FLI-1, PAX3-FKHR, and PAX7-FKHR chimeric transcripts. '), ('10126', 'PAX7_FKHR', '', 'PAX7', 'FKHR', '7495283', '-21', 'alveolar rhabdomyosarcoma;desmoplastic small round cell tumor;ewing sarcoma;neuroectodermal tumor;rhabdomyosarcoma', '', '', '', '', '', '', '', '', 'To investigate the structure and potential diagnostic utility of the detection of EWS-WT1 chimeric RNA in desmoplastic small round cell tumor, 12 examples of this entity and 49 other tumors that enter in its differential diagnosis were studied by reverse transcriptase polymerase chain reaction for the presence of EWS-WT1, EWS-FLI-1, PAX3-FKHR, and PAX7-FKHR chimeric transcripts.     ///    PAX3/PAX7-FKHR chimeras were present in 9 of 13 alveolar rhabdomyosarcomas but not in any other tumors. '), ('10127', 'PAX7_FOXO1A', '', 'PAX7', 'FOXO1A', '22710718', '-21', 'rhabdomyosarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Alveolar rhabdomyosarcoma (ARMS) is an aggressive childhood cancer of striated muscle characterized by the presence of the PAX3-FOXO1A or PAX7-FOXO1A chimeric oncogenic transcription factor.'), ('10128', 'ATIC_ALK', '', 'ATIC', 'ALK', '18572809', '-21', 'anaplastic large cell lymphoma;lymphoma\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', '', 'ATIC-ALK chimeric transcripts were detected by reverse transcriptase polymerase chain reaction. '), ('10129', 'ETV6_AML1', '', 'ETV6', 'AML1', '9664088', '-22', 'acute lymphoblastic leukemia;lymphoblastic leukemia;leukemia\r\r', '', '', '', '', '', '', '', '', 'We have identified a nonapeptide (RIAECILGM), encoded by the fusion region of the ETV6-AML1 protein, that binds to HLA-A2.1 molecules and induces specific primary CTL in peripheral blood lymphocytes from healthy donors.     ///    Cytotoxic T cell response against the chimeric ETV6-AML1 protein in childhood acute lymphoblastic leukemia..     ///    \"In this study, we have examined whether the chimeric ETV6-AML1 protein could serve as a tumor specific antigen for CTL in HLA-A2.1 individuals. \"'), ('10130', 'SYT_SSX2', '', 'SYT', 'SSX2', '11395555', '-22', 'synovial sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'RT-PCR studies for the presence of a SYT-SSX1 or SYT-SSX2 fusion transcript were positive in every tumor.     ///    \"Identification of the synovial sarcoma-specific chimeric transcript (SYT-SSX1 or SYT-SSX2), in conjunction with immunoperoxidase studies, can be extremely helpful in identifying cases of pleural monophasic synovial sarcoma.. \"'), ('10131', 'SYT_SSX1', '', 'SYT', 'SSX1', '11395555', '-22', 'synovial sarcoma;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'RT-PCR studies for the presence of a SYT-SSX1 or SYT-SSX2 fusion transcript were positive in every tumor.     ///    \"Identification of the synovial sarcoma-specific chimeric transcript (SYT-SSX1 or SYT-SSX2), in conjunction with immunoperoxidase studies, can be extremely helpful in identifying cases of pleural monophasic synovial sarcoma.. \"'), ('10132', 'DEK_CAN', '', 'DEK', 'CAN', '8294483', '-22', 'acute myeloid leukemia', '', '', '', '', '', '', '', '', 'This proposed role would therefore be similar to the roles observed for BCR and DEK of the chimeric oncoproteins BCR-ABL and DEK-CAN in acute myeloid leukemia and acute nonlymphocytic leukemia, respectively.. '), ('10133', 'NSE_HIS', '', 'NSE', 'HIS', '17121695', '-23', 'prion disease\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'SDS-PAGE assay yielded an approximately 22 kD HIS-NSE fusion protein.     ///    HIS-NSE fusion protein expression was obtained in E. '), ('10134', 'E2A_PBX1', '', 'E2A', 'PBX1', '11571641', '-23', 'acute myeloid leukemia;myeloid leukemia;leukemia\r\r', '', '', '', '', '', 'Transcription_Factor', '', '', 'E2a-Pbx1, an oncogenic derivative of Pbx1, both retains its ability to heterodimerize with Hox proteins and arrest myeloid differentiation.'), ('10135', 'TMPRSS2_ERG', '', 'TMPRSS2', 'ERG', '17785564', '-25', 'prostate cancer\r\r', 'PCR;RT-PCR', '', '', '', '', '', 'KB', 'Seq', 'In this report, we used for the first time the combination of the prostate cancer-specific biomarkers TMPRSS2-ERG and PCA3, which significantly improves the sensitivity for prostate cancer diagnosis.. '), ('10136', 'EML4_ALK', '', 'EML4', 'ALK', '22483782', '-25', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'Twenty-eight (3.9%) patients harbored the EML4-ALK gene.    ///    Clinicoradiologic characteristics of patients with lung adenocarcinoma harboring EML4-ALK fusion oncogene.    ///    The clinicopathological characteristics of each patient were compared among the subgroups stratified by the EML4-ALK gene status.     ///    We explored the EML4-ALK gene in a relatively large cohort and reviewed the clinicoradiologic background of the patients.     ///    Clinicoradiologic characteristics of patients with lung adenocarcinoma harboring EML4-ALK fusion oncogene..     ///    \"Younger age (p=0.001), no or light history of smoking (p=0.05) and normal serum carcinoembryonic antigen (CEA) level (p=0.04) were characteristics of the patients with EML4-ALK.\"    ///    \"Younger age (p=0.001), no or light history of smoking (p=0.05) and normal serum carcinoembryonic antigen (CEA) level (p=0.04) were characteristics of the patients with EML4-ALK. \"'), ('10137', 'PML_RARA', '', 'PML', 'RARA', '8095167', '-25', 'acute promyelocytic leukemia;leukemia\r\r', '', '', 'Oncogene', '', 'Receptor', 'Transcription_Factor', 'KB', 'Seq', 'Human CD4 lymphocytes specifically recognize a peptide representing the fusion region of the hybrid protein pml/RAR alpha present in acute promyelocytic leukemia cells.. '), ('10138', 'PAX7_FOXO1A', '', 'PAX7', 'FOXO1A', '16157701', '-25', 'rhabdomyosarcoma;sarcoma\r\r', '', '', '', '', '', '', '', '', 'Although both forms of RMS express muscle cell-specific markers, only ARMS cells express PAX3-FOXO1a or PAX7-FOXO1a chimeric proteins.'), ('10139', 'HTERT_IL18', '', 'HTERT', 'IL18', '18226991', '-25', 'leukemia\r\r', 'PCR', '', '', '', '', '', '', '', 'DCs transfected with hTERT-IL18 acquired stronger telomerase activity and were able to elicit an hTERT-specific cytotoxic T lymphocyte CTL response in vitro.     ///    DCs transfected with hTERT-IL18 gene were capable of eliciting a stronger hTERT-specific CTL response in vitro.. '), ('10140', 'WT1_EWS', '', 'WT1', 'EWS', '10989634', '-25', 'ewing sarcoma;neuroectodermal tumor;desmoplastic small round cell tumor;sarcoma\r\r', 'PCR;RT-PCR', '', '', '', '', '', '', '', 'For cases in which the morphologic and immunohistochemical features are consistent with a diagnosis of DSRCT, WT1 antibody staining predicts the EWS-WT1 translocation with high sensitivity and specificity and is, therefore, useful for differentiating DSRCT from EWS/PNET when genetic information is unavailable.. '), ('10141', 'EWSR1_FLI1', '', 'EWSR1', 'FLI1', '18435455', '-25', '', 'PCR;RT-PCR', '', '', '', '', '', 'KB', 'Seq', 'The sensitivity of the LIPI RT-PCR was similar to the sensitivity of the conventional EWSR1-FLI1 RT-PCR, suggesting that LIPI might be useful as additional diagnostic target structure.    ///    \"The sensitivity of the LIPI RT-PCR was similar to the sensitivity of the conventional EWSR1-FLI1 RT-PCR, suggesting that LIPI might be useful as additional diagnostic target structure. \"'), ('10142', 'WAVE2_ABI1', '', 'WAVE2', 'ABI1', '17389688', '-26', 'leukemia\r\r', '', '', '', 'Tumor_suppressor', '', '', '', '', 'Together, these data define Abi1/WAVE2 as a downstream pathway that contributes to Bcr-Abl-induced abnormalities of cytoskeletal and integrin function..     ///    \"Bcr-Abl-induced membrane translocation of Abi1/WAVE2 requires direct interaction between Abi1 and Bcr-Abl, but is independent of the phosphoinositide 3-kinase pathway. \"    ///    \"More importantly, disruption of the interaction between Bcr-Abl and Abi1 by mutations either in Bcr-Abl or Abi1 not only abolished tyrosine phosphorylation of Abi1 and membrane translocation of Abi1/WAVE2, but also inhibited Bcr-Abl-stimulated actin cytoskeleton remodeling, integrin clustering and cell adhesion to fibronectin. \"    ///    \"This is accompanied by a subcellular translocation of Abi1/WAVE2 to a site adjacent to membrane, where an F-actin-enriched structure containing the adhesion molecules such as beta1-integrin, paxillin and vinculin is assembled. \"'), ('10143', 'IL18_EGF', '', 'IL18', 'EGF', '16120577', '-28', '', '', '', '', '', '', '', '', '', 'Furthermore, EGF Receptor competitive test in human epithelial cancer A431 cell line showed that EGF- IL18 fusion protein can specifically bind with EGFR by competing with native EGF protein.     ///    It was proposed that a targeted delivery of IL-18 by generation of IL-18-EGF fusion protein might decrease adverse effects and result in enhancing cytotoxic and antitumor activities.     ///    The results suggested that EGF-IL18 fusion protein could specifically be targeted on tumor cells. '), ('10144', 'TAT_HSP20', '', 'TAT', 'HSP20', '17084643', '-29', '', '', '', '', '', '', '', '', '', 'This phosphorylated TAT-HSP20 was physiologically active in intact smooth muscles in that it inhibited 5-hydroxytryptamine-induced contractions by 57%+/-4.5.     ///    Immunoblot and HPLC-ESI-MS/MS analysis of the purified TAT-HSP20 demonstrated that it was phosphorylated at serine 40 (equivalent to serine 16 in wild-type human HSP20).     ///    \"In this study, we co-expressed in Escherichia coli the cDNAs encoding the catalytic subunit of protein kinase G and a TAT-HSP20 fusion protein composed of the TAT PTD (-YGRKKRRQRRR-) fused to the N-terminus of human HSP20. \"'), ('10145', 'EML4_ALK', '', 'EML4', 'ALK', '22443647', '-30', 'non small cell lung cancer;lung cancer\r\r', '', 'Kinase', 'Oncogene', '', '', '', 'KB', 'Seq', 'The monoclonal antibody to EGFR, cetuximab, improves survival in patients with metastatic NSCLC, and the inhibitor of the echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) fusion protein, crizotinib, has resulted in an unprecedented overall survival advantage in patients harboring the EML4-ALK translocation.    ///    \"The monoclonal antibody to EGFR, cetuximab, improves survival in patients with metastatic NSCLC, and the inhibitor of the echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) fusion protein, crizotinib, has resulted in an unprecedented overall survival advantage in patients harboring the EML4-ALK translocation. \"'), ('10146', 'GAL4_NFKB1', '', 'GAL4', 'NFKB1', '16904943', '-33', '', '', '', '', '', '', 'Transcription_Factor', '', '', 'GAL4-NF-kappaB fusion protein augments transgene expression from neuronal promoters in the rat brain.     ///    GAL4-NF-kappaB fusion protein augments transgene expression from neuronal promoters in the rat brain.. '), ('10147', 'PAX3_FOXO1', '', 'PAX3', 'FOXO1', '22037868', '-34', 'rhabdomyosarcoma;sarcoma\r\r', '', '', 'Oncogene', 'Tumor_suppressor', '', 'Transcription_Factor', 'KB', 'Seq', 'In primary myoblasts, Cnr1 was dispensable for PAX3-FOXO1 to mediate cell proliferation, differentiation, or transformation; however, Cnr1 function was essential to increase the invasive capacity conferred by PAX3-FOXO1 overexpression in these cells.    ///    \"Here, we show that upregulation of the cannabinoid receptor 1 (Cnr1/Cb1) by PAX3-FOXO1 in mouse primary myoblasts and ARMS cell lines, contributes to PAX3-FOXO1 phenotypes, both in vivo and in vitro.\"    ///    Genetic or pharmacologic abrogation of Cnr1 inhibited the enhanced basement membrane invasion induced by PAX3-FOXO1.'), ('10148', 'RANBP2_ALK', '', 'RANBP2', 'ALK', '12661011', '-37', 'dermatofibrosarcoma,', '', 'Kinase', 'Oncogene', '', '', '', 'KB', '', 'The N-terminal 867 residues of RANBP2 are fused to the cytoplasmic segment of ALK in the 1,430-amino acid RANBP2-ALK chimeric protein.     ///    \"Myofibroblasts that express RANBP2-ALK exhibit nuclear membrane-associated ALK staining that is unique compared to the subcellular localization observed with other ALK fusions in IMT, presumably attributable to heteroassociation of the fusion with normal RANBP2 at the nuclear pore. \"'), ('10149', 'MBP_FAAH', '', 'MBP', 'FAAH', '17476568', '-39', '', '', '', '', '', '', '', '', '', 'A MBP-FAAH fusion protein as a tool to produce human and rat fatty acid amide hydrolase: expression and pharmacological comparison.     ///    A MBP-FAAH fusion protein as a tool to produce human and rat fatty acid amide hydrolase: expression and pharmacological comparison.. '), ('10150', 'EWSR1_ERG', '', 'EWSR1', 'ERG', '11823984', '-47', 'ewing sarcoma;sarcoma\r\r', '', '', '', '', '', '', 'KB', 'Seq', 'A reverse transcriptase-polymerase chain reaction followed by sequencing revealed an EWSR1/ERG chimeric transcript, which combined EWSR1 exon 10 with ERG exon 6.     ///    This type of tumor is well characterized by recurrent chromosomal translocation such as t (11;22) (q24;q12) (EWSR1/FLI1) or t (21;22) (q22;q12) (EWSR1/ERG) and overexpression of MIC2/CD99 on tumor cell membrane. '), ('10151', 'NPM_ALK', '', 'NPM', 'ALK', '9777981', '-50', 'lymphoma;lymphoproliferative disorder\r\r', '', 'Kinase', 'Oncogene', '', '', '', '', '', 'Nested reverse transcriptase-polymerase chain reaction allowed the detection of NPM-ALK transcripts in 10 of 26 CD30+ primary and in 3 of 11 secondary cutaneous large-cell lymphomas.     ///    \"In CD30+ primary cutaneous lymphoproliferation, NPM-ALK transcripts might be expressed by very rare normal or tumoral cells that are undetectable by immunohistochemistry. \"    ///    \"However, the expression of either NPM-ALK transcripts or ALK-protein was not correlated with prognosis or age in CD30+ cutaneous lymphoproliferations.. \"');
