Beyond BCL-2: What drives venetoclax resistance in acute myeloid leukemia?
Understanding how leukemia cells escape venetoclax therapy reveals combination strategies to restore drug sensitivity and improve treatment outcomes.
This Cancer Cell perspective catalogues the expanding landscape of venetoclax resistance mechanisms in AML, identifying BCL-family compensation, somatic BAX mutations, mitochondrial structure remodeling, and lineage-associated transcription factor reprogramming as validated or emerging drivers. The authors propose combination strategies targeting metabolic adaptations and call for prospective validation of these putative resistance mechanisms in clinical AML cohorts.
What the study was
- Study design
- Narrative Review / Perspective
- Population
- AML patients on venetoclax-based therapy who develop acquired treatment resistance
- Category
- Treatment Innovation
- Maturity
- Exploratory
- Journal
- Cancer Cell
Why it surfaced
Cancer Cell review on emerging venetoclax resistance mechanisms; highly relevant as venetoclax+azacitidine is now AML SOC and resistance is a major clinical challenge requiring novel combination strategies.
A plain-language summary of published research — not medical advice. Talk to a clinician about your own care.