Targeting p16INK4a-mediated cellular senescence as a therapeutic strategy for FLT3-ITD-driven AML

Zheng J, Jin L, Chen Y, et al

Using multiple sequencing datasets, the authors identified that FLT3-ITD-positive patients with low p16INK4a expression had significantly worse prognoses. According to the authors, the FLT3-ITD-STAT5A/E2F3/EZH2-p16INK4a axis represents a promising target for addressing refractory FLT3-ITD AML with low p16INK4a expression.