Abstract B074: Evaluation of a small molecule, AP-232, as a splicing factor inhibitor of U2 auxiliary factor 1 (U2AF1) in leukemia cells
Enhanced activity in SF3B1-mutant cells suggests that simultaneous targeting of splicing and autophagy dependencies may represent a therapeutic strategy for SF3B1–mutant hematological malignancies, potentially driven by increased reliance on autophagy as a survival mechanism in this genetic context.