Mitochondrial metabolism sustains DNMT3A-R882-mutant clonal haematopoiesis.

doi:10.1038/s41586-025-08980-6

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Article

Mitochondrial metabolism sustains DNMT3A-R882-mutant clonal haematopoiesis.

Nature - 1 Jun 2025

Gozdecka Malgorzata, Dudek Monika, Wen Sean, Gu Muxin, Stopforth Richard J, Rak Justyna, Damaskou Aristi, Grice Guinevere L, McLoughlin Matthew A, Bond Laura, Wilson Rachael, Giotopoulos George, Shanmugiah Vijaya Mahalingam, Bakar Rula Bany, Yankova Eliza, Cooper Jonathan L, Narayan Nisha, Horton Sarah J, Asby Ryan, Pask Dean C, Mupo Annalisa, Duddy Graham, Marando Ludovica, Georgomanolis Theodoros, Carter Paul, Ramesh Amirtha Priya, Dunn William G, Barcena Clea, Gallipoli Paolo, Yusa Kosuke, Petrovski Slavé, Wright Penny, Quiros Pedro M, Frezza Christian, Nathan James A, Kaser Arthur, Kar Siddhartha, Tzelepis Konstantinos, Mitchell Jonathan, Fabre Margarete A, Huntly Brian J P, Vassiliou George S

Abstract excerpt

Somatic DNMT3A-R882 codon mutations drive the most common form of clonal haematopoiesis (CH) and are associated with increased acute myeloid leukaemia (AML) risk1,2. Preventing expansion of DNMT3A-R882-mutant haematopoietic stem/progenitor cells (HSPCs) may therefore avert progression to AML. To identify DNMT3A-R882-mutant-specific vulnerabilities, we conducted a genome-wide CRISPR screen on primary mouse...

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PMID: 40239706
DOI: 10.1038/s41586-025-08980-6
PMCID: PMC12158785

Genes

DNMT3A
SLC25A1

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