 The TEL/AML1 fusion gene which represents the most frequent genetic abnormality in childhood ALL, usually results from genomic breakpoints in TEL intron 5 and AML1 intron 1 or 2.     ///    "This region was supposed to play an important role in TEL/AML1 function, particularly in TEL/AML1-mediated transcriptional repression of AML1 targets. "    ///    "By using reporter gene assay, we showed that the loss of the central region does not influence the TEL/AML1-mediated transcriptional repression. "    ///    The deletion of the central region did not affect the TEL/AML1-specific phenotype.     ///    we did not find any relevant differences in clinical and biological features when variant versus classical TEL/AML1-positive cases were compared.     ///    We aimed at investigating the impact of the loss of this region on disease behavior and TEL/AML1 function.     ///    No distinct differences between variant and classical TEL/AML1 cases were observed including gene expression profiling and detailed immunophenotyping.     ///    "Thus, our data does not support hypothesis that the central region of TEL is indispensable for TEL/AML1 driven leukemogenesis.. "    ///    "We compared clinical and biological characteristics, treatment response, and outcome of the variant versus classical TEL/AML1 cases, analyzed genome wide gene expression profiles and performed reporter gene assay. "    ///    TEL/AML1-positive patients lacking TEL exon 5 resemble canonical TEL/AML1 cases..     ///    We identified two ALL patients with genomic breakpoints within TEL intron 4 resulting in variant TEL/AML1 fusion lacking the TEL exon 5-coded central region. 