Cell Death Discovery· 2026Q1
Anthracycline and antimetabolite, trigger distinct resistance mechanisms in TP53mut AML
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- Q1SCImago
- 2026year
Short summary
TP53-mutated Acute Myeloid Leukemia (AML) exhibits distinct resistance mechanisms to anthracycline and antimetabolite chemotherapies, posing a significant challenge for treatment.
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Key points
- TP53-mutated AML is associated with poor prognosis and resistance to standard chemotherapy.
- TP53 mut AML patients experience lower response rates and higher relapse rates.
- Distinct resistance mechanisms emerge against anthracycline and antimetabolite drugs in TP53 mut AML.
AI-generated from the title and abstract; the full text is not read.
Abstract
Acute myeloid leukemia (AML) is a highly heterogeneous and extremely aggressive form of blood cancer. Despite recent advances, AML continues to be a challenging disease to treat; the overall prognosis and response to therapy are strongly influenced by karyotypic and molecular alterations [ 1 ]. Mutations of the Tp53 gene ( TP53 mut ) are among the most common alterations found in human malignancies, affecting 5–20% of de novo AML and more frequently (up to 37%) observed in patients with therapy-related AML [ 1 , 2 ]. The TP53 mut AML has also been associated with a lower response to conventional chemotherapies, high relapse, and inferior overall survival [ 2 , 3 , 4 ]. Since 2017, the Food and Drug Administration (FDA) has approved several new drugs for AML [ 1 ], but treating TP53 muts AML remains a formidable challenge.
The authors' abstract, as published at the source. Cell Death Discovery, 2026 · DOI ↗
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Field: Hematology
HematologyMedicine