GSE111917
RUNX1 mutations lead to a myeloid differentiation block by altering the RUNX1 transcriptional program (ChIP-Seq)
Mutations in the RUNX1 gene (RUNX1mut) have been established in myelodysplasia (MDS), de novo and secondary acute myeloid leukaemia (AML), and are in general associated with an unfavourable clinical outcome. Familial RUNX1 mutations are associated with familial thrombocytopenia and these patients have a predisposition to AML development. However, a number of studies have been performed so far in mice which might be distinct from the human hematopoietic system. Therefore we studied the cellular phenotypes, the RUNX1 binding pattern and expression profile induced by RUNX1mut in cord blood (CB) CD34+ cells and induced pluripotent stem cell (iPSC) and compared these findings to primary RUNX1mut AML's. Overall design: A total of six samples were subject to ChIP-Seq including control and RUNX1mut-transduced groups in cord blood CD34 cells as well as time-course iPSCs.