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PML targeting eradicates quiescent leukaemia-initiating cells

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  • Keisuke Ito

    (Cancer Genetics Program, Beth Israel Deaconess Cancer Center
    Cancer Biology and Genetics Program,
    Memorial Sloan-Kettering Cancer Center, Sloan-Kettering Institute, 1275 York Avenue, New York, New York 10021, USA)

  • Rosa Bernardi

    (Cancer Genetics Program, Beth Israel Deaconess Cancer Center
    Cancer Biology and Genetics Program,
    Memorial Sloan-Kettering Cancer Center, Sloan-Kettering Institute, 1275 York Avenue, New York, New York 10021, USA)

  • Alessandro Morotti

    (Cancer Genetics Program, Beth Israel Deaconess Cancer Center
    Cancer Biology and Genetics Program,
    Memorial Sloan-Kettering Cancer Center, Sloan-Kettering Institute, 1275 York Avenue, New York, New York 10021, USA)

  • Sahoko Matsuoka

    (Keio University School of Medicine, 35 Shinano-machi, Shinjuku-ku, Tokyo 160-8582, Japan)

  • Giuseppe Saglio

    (University of Turin)

  • Yasuo Ikeda

    (Keio University School of Medicine, 35 Shinano-machi, Shinjuku-ku, Tokyo 160-8582, Japan)

  • Jacalyn Rosenblatt

    (Beth Israel Deaconess Medical Center, Harvard Medical School, New Research Building, 330 Brookline Avenue, Boston, Massachusetts 02215, USA)

  • David E. Avigan

    (Beth Israel Deaconess Medical Center, Harvard Medical School, New Research Building, 330 Brookline Avenue, Boston, Massachusetts 02215, USA)

  • Julie Teruya-Feldstein

    (Memorial Sloan-Kettering Cancer Center, Sloan-Kettering Institute, 1275 York Avenue, New York, New York 10021, USA)

  • Pier Paolo Pandolfi

    (Cancer Genetics Program, Beth Israel Deaconess Cancer Center
    Cancer Biology and Genetics Program,
    Memorial Sloan-Kettering Cancer Center, Sloan-Kettering Institute, 1275 York Avenue, New York, New York 10021, USA)

Abstract

The existence of a small population of ‘cancer-initiating cells’ responsible for tumour maintenance has been firmly demonstrated in leukaemia. This concept is currently being tested in solid tumours. Leukaemia-initiating cells, particularly those that are in a quiescent state, are thought to be resistant to chemotherapy and targeted therapies, resulting in disease relapse. Chronic myeloid leukaemia is a paradigmatic haematopoietic stem cell disease in which the leukaemia-initiating-cell pool is not eradicated by current therapy, leading to disease relapse on drug discontinuation. Here we define the critical role of the promyelocytic leukaemia protein (PML) tumour suppressor in haematopoietic stem cell maintenance, and present a new therapeutic approach for targeting quiescent leukaemia-initiating cells and possibly cancer-initiating cells by pharmacological inhibition of PML.

Suggested Citation

  • Keisuke Ito & Rosa Bernardi & Alessandro Morotti & Sahoko Matsuoka & Giuseppe Saglio & Yasuo Ikeda & Jacalyn Rosenblatt & David E. Avigan & Julie Teruya-Feldstein & Pier Paolo Pandolfi, 2008. "PML targeting eradicates quiescent leukaemia-initiating cells," Nature, Nature, vol. 453(7198), pages 1072-1078, June.
    • Handle: RePEc:nat:nature:v:453:y:2008:i:7198:d:10.1038_nature07016
    DOI: 10.1038/nature07016
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    Cited by:

    1. Sarah Tessier & Omar Ferhi & Marie-Claude Geoffroy & Román González-Prieto & Antoine Canat & Samuel Quentin & Marika Pla & Michiko Niwa-Kawakita & Pierre Bercier & Domitille Rérolle & Marilyn Tirard &, 2022. "Exploration of nuclear body-enhanced sumoylation reveals that PML represses 2-cell features of embryonic stem cells," Nature Communications, Nature, vol. 13(1), pages 1-15, December.

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