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CLONAL HEMATOPOIESIS

Multi-omics on our multitudes

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Clonal expansion of DNMT3A-mutant hematopoietic stem cells is a risk factor for myeloid malignancies and other morbidities. A new study uses multi-modal single-cell genomics to characterize the myeloid differentiation bias of DNMT3A-mutated clones, and finds preferential hypomethylation of binding motifs for key transcriptional regulators.

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Fig. 1: Single-cell multi-omic analyses show how DNMT3A R882 mutations bias hematopoietic fate decisions.

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Authors and Affiliations

  1. Division of Hematology/Oncology, Boston Children’s Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA

    Richard A. Voit & Vijay G. Sankaran

  2. Broad Institute of MIT and Harvard, Cambridge, MA, USA

    Richard A. Voit & Vijay G. Sankaran

Authors
  1. Richard A. Voit
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  2. Vijay G. Sankaran
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Correspondence to Vijay G. Sankaran.

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Competing interests

V.G.S. serves as an advisor to and/or has equity in Branch Biosciences, Ensoma, Novartis, Forma and Cellarity, all unrelated to the present work. The authors have no other competing interests to declare.

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Voit, R.A., Sankaran, V.G. Multi-omics on our multitudes. Nat Genet 54, 1449–1450 (2022). https://doi.org/10.1038/s41588-022-01175-z

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  • DOI: https://doi.org/10.1038/s41588-022-01175-z

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