Hotspot DNMT3A mutations in clonal hematopoiesis and acute myeloid leukemia sensitize cells to azacytidine via viral mimicry response.

doi:10.1038/s43018-021-00213-9

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Hotspot DNMT3A mutations in clonal hematopoiesis and acute myeloid leukemia sensitize cells to azacytidine via viral mimicry response.

Nature cancer - 1 May 2021

Scheller Marina, Ludwig Anne Kathrin, Göllner Stefanie, Rohde Christian, Krämer Stephen, Stäble Sina, Janssen Maike, Müller James-Arne, He Lixiazi, Bäumer Nicole, Arnold Christian, Gerß Joachim, Schönung Maximilian, Thiede Christian, Niederwieser Christian, Niederwieser Dietger, Serve Hubert, Berdel Wolfgang E, Thiem Ulrich, Hemmerling Inga, Leuschner Florian, Plass Christoph, Schlesner Matthias, Zaugg Judith, Milsom Michael D, Trumpp Andreas, Pabst Caroline, Lipka Daniel B, Müller-Tidow Carsten

Abstract excerpt

Somatic mutations in DNA methyltransferase 3A (DNMT3A) are among the most frequent alterations in clonal hematopoiesis (CH) and acute myeloid leukemia (AML), with a hotspot in exon 23 at arginine 882 (DNMT3AR882). Here, we demonstrate that DNMT3AR882H-dependent CH and AML cells are specifically susceptible to the hypomethylating agent azacytidine (AZA). Addition of AZA to chemotherapy prolonged AML survival...

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PMID: 35122024
DOI: 10.1038/s43018-021-00213-9

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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