 A reciprocal translocation involving chromosomes 8 and 21 generates the AML1/ETO oncogenic transcription factor that initiates acute myeloid leukemia by recruiting co-repressor complexes to DNA.     ///    Genome-wide chromatin immunoprecipitation and expression profiling were exploited to identify AML1/ETO-dependent transcriptional regulation.     ///    "AML1/ETO interferes with the function of its wild-type counterpart, AML1, by directly targeting AML1 binding sites. "    ///    AML1/ETO oncoprotein is directed to AML1 binding regions and co-localizes with AML1 and HEB on its targets..     ///    "Furthermore, the level of HEB protein was increased in both primary cells and cell lines expressing AML1/ETO. "    ///    "The DNA binding profile of the E-protein HEB was grossly rearranged upon expression of AML1/ETO, and the fusion protein was found to co-localize with both AML1 and HEB on many of its regulated targets. "    ///    "However, transcriptional regulation determined by AML1/ETO probably relies on a more complex network, since the fusion protein has been shown to interact with a number of other transcription factors, in particular E-proteins, and may therefore target other sites on DNA. "    ///    Our results suggest a major role for the functional interaction of AML1/ETO with AML1 and HEB in transcriptional regulation determined by the fusion protein..     ///    "AML1/ETO was found to co-localize with AML1, demonstrating that the fusion protein follows the binding pattern of the wild-type protein but does not function primarily by displacing it. "