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Role of TP53 mutations in the origin and evolution of therapy-related acute myeloid leukaemia

Author

Listed:
  • Terrence N. Wong

    (Washington University)

  • Giridharan Ramsingh

    (University of Southern California)

  • Andrew L. Young

    (Washington University)

  • Christopher A. Miller

    (The Genome Institute, Washington University)

  • Waseem Touma

    (Washington University)

  • John S. Welch

    (Washington University
    Siteman Cancer Center, Washington University)

  • Tamara L. Lamprecht

    (Washington University)

  • Dong Shen

    (AstraZeneca)

  • Jasreet Hundal

    (The Genome Institute, Washington University)

  • Robert S. Fulton

    (The Genome Institute, Washington University)

  • Sharon Heath

    (Washington University)

  • Jack D. Baty

    (Washington University)

  • Jeffery M. Klco

    (Washington University)

  • Li Ding

    (Washington University
    Siteman Cancer Center, Washington University)

  • Elaine R. Mardis

    (The Genome Institute, Washington University
    Siteman Cancer Center, Washington University
    Washington University)

  • Peter Westervelt

    (Washington University
    Siteman Cancer Center, Washington University)

  • John F. DiPersio

    (Washington University
    Siteman Cancer Center, Washington University)

  • Matthew J. Walter

    (Washington University
    Siteman Cancer Center, Washington University)

  • Timothy A. Graubert

    (Washington University
    Siteman Cancer Center, Washington University)

  • Timothy J. Ley

    (Washington University
    Siteman Cancer Center, Washington University)

  • Todd E. Druley

    (Washington University)

  • Daniel C. Link

    (Washington University
    Siteman Cancer Center, Washington University)

  • Richard K. Wilson

    (The Genome Institute, Washington University
    Siteman Cancer Center, Washington University
    Washington University)

Abstract

Somatic TP53 mutations are highly prevalent in therapy-related acute myeloid leukaemia and myelodysplastic syndrome, which arise as complications of cytotoxic chemotherapy or radiotherapy; although it was believed that these TP53 mutations are directly induced by cytotoxic therapy, new data indicate that they predate cytotoxic therapy and that haematopoietic progenitors harbouring these pre-existing mutations may selectively expand after exposure to chemotherapy or radiotherapy.

Suggested Citation

  • Terrence N. Wong & Giridharan Ramsingh & Andrew L. Young & Christopher A. Miller & Waseem Touma & John S. Welch & Tamara L. Lamprecht & Dong Shen & Jasreet Hundal & Robert S. Fulton & Sharon Heath & J, 2015. "Role of TP53 mutations in the origin and evolution of therapy-related acute myeloid leukaemia," Nature, Nature, vol. 518(7540), pages 552-555, February.
    • Handle: RePEc:nat:nature:v:518:y:2015:i:7540:d:10.1038_nature13968
    DOI: 10.1038/nature13968
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    Cited by:

    1. Eline J. M. Bertrums & Jurrian K. Kanter & Lucca L. M. Derks & Mark Verheul & Laurianne Trabut & Markus J. Roosmalen & Henrik Hasle & Evangelia Antoniou & Dirk Reinhardt & Michael N. Dworzak & Nora Mü, 2024. "Selective pressures of platinum compounds shape the evolution of therapy-related myeloid neoplasms," Nature Communications, Nature, vol. 15(1), pages 1-16, December.

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