Journal
BEST PRACTICE & RESEARCH CLINICAL HAEMATOLOGY
Volume 32, Issue 2, Pages 134-144Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.beha.2019.05.004
Keywords
Acute myeloid leukemia (AML); TP53; therapy-related acute myeloid leukemia (t-AML)
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Funding
- Celgene
- Jazz
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Mutations in the essential tumor suppressor gene, TP53, are observed in only 5-10% of acute myeloid leukemia (AML) cases, but are highly associated with therapy-related AML and cases with complex karyotype. The mutational status of TP53 is a critical prognostic indicator, with dismal outcomes consistently observed across studies. Response rates to traditional cytotoxic chemotherapy are poor and long-term survival after allogeneic hematopoietic stem cell transplant is rare. Therapy with hypomethylating agents has resulted in a modest improvement in outcomes over intensive chemotherapy, but durable responses are seldom observed. In view of the intrinsic resistance to standard chemotherapies conferred by mutations in TP53, novel treatment approaches are required. In this review, we examine the current treatment landscape in TP53 mutated AML and discuss emerging therapeutic approaches currently under clinical investigation.
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