Combinatorial DNMTs and EZH2 inhibition reprograms the H3K27me3 and DNAme-mediated onco-epigenome to suppress multiple myeloma proliferation
Comprehensive epigenomic studies in multiple myeloma (MM) that unravel the connections between major epigenetic regulators, their intertwined collaboration and the potential of combinatorial targeting remain limited. Utilizing ChIP-seq, ATAC-seq, RNA-seq, and DNA methylation (DNAme) data, we generated whole-genome chromatin annotations from normal plasma cells and MM patients, revealing epigenomic
