GSE111821
Genome-wide RUNX1 binding landscape in AMLs with RUNX1 mutation
Analyses of 38 AML samples through integrated multiple epigenomic analysis exposes two major epigenetic subtypes. We found that the majority of patients in an AML subtype have molecular aberrations associated with RUNX1 and splicing factors. Despite this heterogeneity, they give rise to a comparable epigenome, suggesting a common deregulation of the epigenome. Given that differentially spliced genes could result in truncated proteins and/or reduced protein levels, we speculated that mutated RUNX1 protein might deregulate the same genes targeted by mutated spliceosome factors. To explore this option, we performed genome-wide binding analysis of RUNX1 in the RUNX1 mutant (RUNX1mt) expressing AMLs, and analyzed its relationship with previous epigenetic results in our study. Overall design: Four AML samples carrying RUNX1 mutation were sequenced