Depletion of RUNX1/ETO in t(8:21) AML cells leads to genome-wide changes in transcription factor binding

The t(8:21) translocation is present in approximately 15% of all acute myeloid leukemia (AML) cases. This fusion protein is a leukaemia-initiating transcription factor that interferes with RUNX1 function, resulting in a block in differentiation and in the development of AML. However the molecular details of the mechanism of deregulation are still obscure. It is important to identify RUNX1/ETO target sites at the genome-wide level, to define its individual role in reprogramming gene expression networks. To this end we performed Chip-sequencing and found peaks located in already established RUNX1/ETO target genes…