PRDM16 Induces Methylation of FLT3 to Promote FLT3-ITD Signaling and Leukemia Progression

Investigators revealed that genetic and pharmacological suppression of PRDM16 greatly slowed the progression of FMS-like receptor tyrosine kinase-3-internal tandem duplication (FLT3-ITD)-driven leukemia, sensitized leukemic cells to tyrosine kinase inhibitors, and extended the survival of leukemic mice.