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A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia

Author

Listed:
  • Apostolos Klinakis

    (Biomedical Research Foundation, Academy of Athens)

  • Camille Lobry

    (New York University School of Medicine)

  • Omar Abdel-Wahab

    (Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan-Kettering Cancer Center)

  • Philmo Oh

    (New York University School of Medicine)

  • Hiroshi Haeno

    (Dana-Farber Cancer Institute, Harvard School of Public Health)

  • Silvia Buonamici

    (New York University School of Medicine
    Novartis Institutes for Biomedical Research)

  • Inge van De Walle

    (Microbiology and Immunology, Ghent University Hospital, Ghent University)

  • Severine Cathelin

    (New York University School of Medicine)

  • Thomas Trimarchi

    (New York University School of Medicine)

  • Elisa Araldi

    (New York University School of Medicine)

  • Cynthia Liu

    (New York University School of Medicine)

  • Sherif Ibrahim

    (New York University School of Medicine)

  • Miroslav Beran

    (M.D. Anderson Cancer Center)

  • Jiri Zavadil

    (NYU Cancer Institute and Center for Health Informatics and Bioinformatics, NYU Langone Medical Center)

  • Argiris Efstratiadis

    (Biomedical Research Foundation, Academy of Athens)

  • Tom Taghon

    (Microbiology and Immunology, Ghent University Hospital, Ghent University)

  • Franziska Michor

    (Dana-Farber Cancer Institute, Harvard School of Public Health)

  • Ross L. Levine

    (Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan-Kettering Cancer Center)

  • Iannis Aifantis

    (New York University School of Medicine)

Abstract

Notch signalling and tumour suppression Activating mutations in the Notch pathway promote tumorigenesis in T-cell leukaemias. Iannis Aifantis and colleagues now find that the same pathway suppresses the development of myeloid leukaemias. Inactivating the pathway in haematopoietic stem cells leads to myeloid disease resembling chronic myelomonocytic leukaemia (CMML), and mutations in Notch pathway genes can be found in patients with CMML. The Notch pathway is shown to suppress a myeloid differentiation program. These findings demonstrate that the Notch pathway exerts both oncogenic and tumour-suppressor functions in the haematopoietic system and regulates critical cell-fate decisions.

Suggested Citation

  • Apostolos Klinakis & Camille Lobry & Omar Abdel-Wahab & Philmo Oh & Hiroshi Haeno & Silvia Buonamici & Inge van De Walle & Severine Cathelin & Thomas Trimarchi & Elisa Araldi & Cynthia Liu & Sherif Ib, 2011. "A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia," Nature, Nature, vol. 473(7346), pages 230-233, May.
    • Handle: RePEc:nat:nature:v:473:y:2011:i:7346:d:10.1038_nature09999
    DOI: 10.1038/nature09999
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    Cited by:

    1. Laure Talarmain & Matthew A. Clarke & David Shorthouse & Lilia Cabrera-Cosme & David G. Kent & Jasmin Fisher & Benjamin A. Hall, 2022. "HOXA9 has the hallmarks of a biological switch with implications in blood cancers," Nature Communications, Nature, vol. 13(1), pages 1-10, December.

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