Anthracycline and antimetabolite, trigger distinct resistance mechanisms in TP53mut AML

Sanjeev Raghuwanshi; Andrei L. Gartel

doi:10.1038/s41420-026-03352-z

September 17, 2026Cell Death DiscoveryOpen Access

Anthracycline and antimetabolite, trigger distinct resistance mechanisms in TP53mut AML

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Key Points

Characterize the distinct mechanisms driving chemotherapy resistance to anthracyclines and antimetabolites in TP53-mutated acute myeloid leukemia.
Evaluated resistance phenotypes and therapeutic response in TP53-mutated acute myeloid leukemia models treated with conventional chemotherapeutic agents.
Mutations in TP53 occur in 5% to 20% of de novo cases and up to 37% of therapy-related acute myeloid leukemia cases.
TP53-mutated disease confers high resistance to conventional anthracycline and antimetabolite treatments, correlating with high relapse rates and poor overall survival.

Implication

Molecular investigation reveals distinct resistance pathways triggered by anthracycline and antimetabolite therapies in TP53-mutated acute myeloid leukemia, highlighting barriers to standard care.

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Cite This Study

Raghuwanshi et al. (2026) studied this question.

synapsesocial.com/papers/6aad0b22de0393d728b896df https://doi.org/10.1038/s41420-026-03352-z

View Full Paper

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Anthracycline and antimetabolite, trigger distinct resistance mechanisms in TP53mut AML

Key Points

Implication

Discussion

Cite This Study

Anthracycline and antimetabolite, trigger distinct resistance mechanisms in TP53mut AML

Key Points

Implication

Discussion

Cite This Study

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