Acute myeloid leukemia with TP53 mutation: molecular mechanisms and therapeutic advances.

Authors

Zixin Chen, Lin Chen

Published in

Leukemia & lymphoma. Pages 1-11. Nov 13, 2026. Epub Nov 13, 2026.

Abstract

TP53-mutated acute myeloid leukemia (AML) accounts for approximately 5%-10% of newly diagnosed AML. It is characterized by enrichment of complex karyotypes, genomic instability, and treatment resistance, resulting in an extremely poor overall prognosis. Although intensive chemotherapy and hypomethylating agents (HMAs) combined with venetoclax can induce remission in some patients, remission duration and long-term survival remain unsatisfactory; novel treatments targeting the p53 pathway, immune microenvironment, and metabolic vulnerabilities have likewise not achieved a breakthrough. Recent studies indicate that the biological effects of TP53 abnormalities depend not only on the mutation itself but also on allelic status, clonal evolution, cytogenetic background, and the immune and metabolic microenvironments. This review summarizes the molecular features, clonal evolution, immune microenvironment, and metabolic reprogramming of TP53-mutated AML; its biological mechanisms, prognostic implications, and therapeutic advances; and the major challenges of allogeneic hematopoietic stem cell transplantation and novel therapeutic strategies.

PMID:
43031311
Bibliographic data and abstract were imported from PubMed on 14 Nov 2026.

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