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Inflammation drives pressure on TP53 mutant clones in myeloproliferative neoplasms

Nature Genetics volume 55, pages 1432–1434 (2023)Cite this article

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Transformation of a myeloproliferative neoplasm to a secondary acute myeloid leukemia is rare but devastating. Single-cell, multi-omic characterization of hematopoietic stem and progenitor cells now shows the role of inflammation in transformation driven by mutations in TP53, with effects on the mutant clone but also non-mutant counterparts.

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Fig. 1: Genetic evolution of HSPCs during leukemic transformation driven by TP53 mutations.

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Authors and Affiliations

  1. Oncode Institute, Erasmus MC, Rotterdam, The Netherlands

    Adam Benabid & Rebekka K. Schneider

  2. Department of Cell and Tumor Biology; Medical Faculty, RWTH Aachen University, Aachen, Germany

    Adam Benabid & Rebekka K. Schneider

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  1. Adam Benabid
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  2. Rebekka K. Schneider
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Correspondence to Rebekka K. Schneider.

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The authors declare no competing interests.

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Benabid, A., Schneider, R.K. Inflammation drives pressure on TP53 mutant clones in myeloproliferative neoplasms. Nat Genet 55, 1432–1434 (2023). https://doi.org/10.1038/s41588-023-01479-8

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