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TGF-β–FOXO signalling maintains leukaemia-initiating cells in chronic myeloid leukaemia

Author

Listed:
  • Kazuhito Naka

    (Center for Cancer and Stem Cell Research, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa 920-0934, Japan)

  • Takayuki Hoshii

    (Center for Cancer and Stem Cell Research, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa 920-0934, Japan)

  • Teruyuki Muraguchi

    (Center for Cancer and Stem Cell Research, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa 920-0934, Japan)

  • Yuko Tadokoro

    (Center for Cancer and Stem Cell Research, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa 920-0934, Japan)

  • Takako Ooshio

    (Center for Cancer and Stem Cell Research, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa 920-0934, Japan
    Core Research for Evolution Science and Technology (CREST), Japan Science and Technology Agency (JST), Chiyoda-ku, Tokyo 102-0075, Japan)

  • Yukio Kondo

    (Cellular Transplantation Biology, Kanazawa University, Graduate School of Medical Science, Kanazawa, Ishikawa 920-8641, Japan)

  • Shinji Nakao

    (Cellular Transplantation Biology, Kanazawa University, Graduate School of Medical Science, Kanazawa, Ishikawa 920-8641, Japan)

  • Noboru Motoyama

    (National Institute for Longevity Sciences, National Center for Gerontology and Geriatrics, Obu, Aichi 474-8522, Japan)

  • Atsushi Hirao

    (Center for Cancer and Stem Cell Research, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa 920-0934, Japan
    Core Research for Evolution Science and Technology (CREST), Japan Science and Technology Agency (JST), Chiyoda-ku, Tokyo 102-0075, Japan)

Abstract

Leukaemia recurrence Chronic myeloid leukaemia (CML) is caused by a BCR-ABL fusion that generates a constitutively active tyrosine kinase. Although inhibition of tyrosine kinase with imatinib has been used successfully for CML therapy, it does not deplete the leukaemia-initiating cells (LICs) that drive the recurrence of CML. Naka et al. show that Foxo3a plays an essential role in the maintenance of LICs in CML, and that TGF-β is a critical regulator of Akt activation in LICs and controls Foxo3a localization. They also show that treatment of LICs in human CML with a TGF-β inhibitor impairs their colony-forming ability in vitro.

Suggested Citation

  • Kazuhito Naka & Takayuki Hoshii & Teruyuki Muraguchi & Yuko Tadokoro & Takako Ooshio & Yukio Kondo & Shinji Nakao & Noboru Motoyama & Atsushi Hirao, 2010. "TGF-β–FOXO signalling maintains leukaemia-initiating cells in chronic myeloid leukaemia," Nature, Nature, vol. 463(7281), pages 676-680, February.
    • Handle: RePEc:nat:nature:v:463:y:2010:i:7281:d:10.1038_nature08734
    DOI: 10.1038/nature08734
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    Cited by:

    1. Junho Lee & Donggu Lee & Sean Lawler & Yangjin Kim, 2021. "Role of neutrophil extracellular traps in regulation of lung cancer invasion and metastasis: Structural insights from a computational model," PLOS Computational Biology, Public Library of Science, vol. 17(2), pages 1-29, February.
    2. Yinzhe GE & Mang XIAO, 2019. "Chronic Myeloid Leukemia: How to Overcome the Tyrosine Kinase Inhibitors Resistance," Biomedical Journal of Scientific & Technical Research, Biomedical Research Network+, LLC, vol. 18(2), pages 13389-13393, May.

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