Jean M G Sabile, Ronan Swords, Jeffrey W Tyner
Mutation of thetumor suppressor gene, TP53 ( tumor protein 53 ), occurs in up to 15% of all patients with acute myeloid leukemia (AML) and is enriched within specific clinical subsets, most notably in older adults, and including secondary AML cases arising from preceding myeloproliferative neoplasm (MPN), myelodysplastic syndrome (MDS), patients exposed to prior DNA-damaging, cytotoxic therapies. In all cases, these tumors have remained difficult to effectively treat with conventional therapeutic regimens. Newer approaches fortreatmentof TP53- mutated AML have shifted to interventions that maymodulate TP53 function, target downstream molecular vulnerabilities, target non-p53 dependent molecular pathways, and/or elicit immunogenic responses...
April 22, 2024: Leukemia & Lymphoma