Clonal Evolution of PPM1D Mutations in the Spectrum of Myeloid Disorders.

Date publication

juin 2025

Journal

Clinical cancer research : an official journal of the American Association for Cancer Research

Auteurs

Membres identifiés du Cancéropôle Est :
Dr MARCAIS Ambroise

Tous les auteurs :
Fandrei D, Pegliasco J, Pasquier F, Ibrahim N, Kfoury M, Berthon C, Heiblig M, Lebon D, Marçais A, Meunier M, Al Jijakli A, Lemasle E, Chantepie S, Pautas C, Dumas PY, Salanoubat C, Carp D, Loyaux R, Quivoron C, Pages A, Job B, Jelin R, Jules-Clement G, Antony-Debré I, Renneville A, Cotteret S, Itzykson R, Dombret H, Duployez N, Droin N, Leary A, Marzac C, Bernard E, Micol JB

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/40162927

Résumé

PPM1D, a central regulator of the DNA damage response, is commonly mutated in therapy-related clonal hematopoiesis, acute myeloid leukemia (AML), and myelodysplastic syndromes (MDS). PPM1D mutations have been shown to expand under the selective pressure of DNA-damaging chemotherapy. However, whether PPM1D mutations promote the development of hematologic malignancies remains unclear.

Mots clés

Humans, Protein Phosphatase 2C, genetics, Clonal Evolution, genetics, Mutation, Female, Male, Middle Aged, Aged, Leukemia, Myeloid, Acute, genetics, Myelodysplastic Syndromes, genetics, Adult, Tumor Suppressor Protein p53, genetics, Aged, 80 and over, Single-Cell Analysis, DNA Methyltransferase 3A, Clonal Hematopoiesis, genetics

Référence

Clin Cancer Res. 2025 06 3;31(11):2241-2253