Oncogenesis and organ infiltration specific therapy in a preclinical model of Ph-like B cell acute lymphoblastic leukemia [RNA-seq dataset 1]

We investigated whether IRF4 deletion might have other collateral oncogenic effects, e.g. by causing signaling pathway alterations and transcriptional changes involved in leukemogenesis. In a first step, we therefore compared gene expression of tumours 10, 11 and 14 described above to those of B220+ mIgM- pro/preB cells that had been sorted from the BM of Irf4–/– mice. The genes that differed more than two-fold between samples were then, in a second step, reduced to only those that we found to be altered by de novo IRF4 expression (Fig. 3E). This approach allowed us to focus on genes that are regulated by IRF4 and at the same time altered in leukemic as compared to non-transformed pro/preB cells. Finally, as a further level of selection, the resulting genes were matched with a data bank provided by Ochiai et al. and selected for genes bound by IRF4 in a ChIP analysis of B cells. Examination of primary Irf4–/– leukemia samples in comparison to Irf4–/– bone marrow derived pro/preB cells, as well as leukemia cell lines retrovirally transduced with empty vector control or IRF4 coding retrovirus.