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Abstract
B-cell lymphoma 2 (BCL-2) was discovered at the breakpoint of the t(14;18) in follicular lymphoma >30 years ago. Although inhibition of BCL-2 first proved valuable in lymphoid malignancies, clinical progress in myeloid malignancies lagged. Here, we summarize the basic biology and preclinical results that spurred clinical BCL-2 inhibition in acute myeloid leukemia (AML). Response rates and toxicity for venetoclax in combination with standard AML agents, such as azacitidine, decitabine, and low-dose cytarabine, compare favorably with conventional induction chemotherapy. Durability of response requires further study.
- Submitted March 16, 2018.
- Accepted July 6, 2018.
- © 2018 by The American Society of Hematology
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Volume: 132
Issue: 10
Pages: 1007-1012
DOI: https://doi.org/10.1182/blood-2018-03-828269
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