Herein, we focus on the role of single-agent BCL-2 inhibition in AML and review the clinical studies of venetoclax-based combination regimens and the evolving mechanisms of resistance.
In this issue of Cancer Cell, Pan et al. show that a combination therapy designed to reactivate the p53 tumor suppressor while antagonizing the anti-apoptotic function of Bcl-2 is highly active in preclinical models of refractory acute myeloid leukemia (AML).
The apoptosis of the AML cell line, U937, was assessed by MTT and Hoechst staining, the expression of Bcl-2, caspases-3 and -9, hypoxia-inducible factor 1α (HIF‑1α) and its target gene GLUT-1, were assayed by western blotting and the role of HIF‑1α was evaluated through siRNA.
Bcl-2 expression showed a prognostic value in our patients indicating that even despite of some differences in treatment regimen, immunocytochemical analysis of this marker is still a simple and inexpensive method for evaluation of prognosis in AML patients.