CBFB-MYH11 directly activates TGFβ and PD-L1 to drive immune evasion in acute myeloid leukemia

Background

Core binding factor acute myeloid leukemia (CBF-AML) driven by the CBFB-MYH11 fusion oncogene is associated with high initial remission rates, yet 30%–50% of patients ultimately relapse. While immune evasion is a recognized hallmark of leukemia progression, the precise mechanisms orchestrated by the CBFB-MYH11 oncogene remain poorly understood. Furthermore, the role of transforming growth factor-beta (TGFβ) in hematological malignancies is highly controversial, often viewed as a tumor suppressor in early hematopoiesis rather than a driver of immune evasion.