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Gain-of-function of mutated C-CBL tumour suppressor in myeloid neoplasms

Author

Listed:
  • Masashi Sanada

    (Cancer Genomics Project,
    Core Research for Evolutional Science and Technology,)

  • Takahiro Suzuki

    (Jichi Medical University, 3311-1 Yakushiji, Shimotsuke-shi, Tochigi 329-0498, Japan)

  • Lee-Yung Shih

    (Chang Gung Memorial Hospital, Chang Gung University, 199 Tung Hwa North Road, Taipei 105, Taiwan)

  • Makoto Otsu

    (Center for Stem Cell and Regenerative Medicine)

  • Motohiro Kato

    (Cancer Genomics Project,
    Department of Pediatrics,)

  • Satoshi Yamazaki

    (Exploratory Research for Advanced Technology, Japan Science and Technology Agency, 4-1-8 Honcho, Kawaguchi-shi, Saitama 332-0012, Japan)

  • Azusa Tamura

    (Cancer Genomics Project,)

  • Hiroaki Honda

    (Research Institute of Radiation Biology and Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan)

  • Mamiko Sakata-Yanagimoto

    (Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Tennodai, Tukuba-shi, Ibaraki, 305-8571, Japan)

  • Keiki Kumano

    (Cell Therapy and Transplantation Medicine, and,)

  • Hideaki Oda

    (Tokyo Women’s Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan)

  • Tetsuya Yamagata

    (Dokkyo University School of Medicine, 800 Kitabayashi, Mibu, Tochigi 321-0293, Japan)

  • Junko Takita

    (Cancer Genomics Project,
    Department of Pediatrics,
    Cell Therapy and Transplantation Medicine, and,)

  • Noriko Gotoh

    (Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan)

  • Kumi Nakazaki

    (Cancer Genomics Project,
    Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan)

  • Norihiko Kawamata

    (Hematology/Oncology, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048, USA)

  • Masafumi Onodera

    (National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo, 157-8535, Japan)

  • Masaharu Nobuyoshi

    (Jichi Medical University, 3311-1 Yakushiji, Shimotsuke-shi, Tochigi 329-0498, Japan)

  • Yasuhide Hayashi

    (Gunma Children’s Medical Center, 779 Shimohakoda, Hokkitsu-machi, Shibukawa-shi, Gunma 377-8577, Japan)

  • Hiroshi Harada

    (Internal Medicine, Showa University Fujigaoka Hospital, 1-30 Fujigaoka, Aoba-ku, Yokohama, Kanagawa 227-8501, Japan)

  • Mineo Kurokawa

    (Cell Therapy and Transplantation Medicine, and,
    Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan)

  • Shigeru Chiba

    (Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Tennodai, Tukuba-shi, Ibaraki, 305-8571, Japan)

  • Hiraku Mori

    (Internal Medicine, Showa University Fujigaoka Hospital, 1-30 Fujigaoka, Aoba-ku, Yokohama, Kanagawa 227-8501, Japan)

  • Keiya Ozawa

    (Jichi Medical University, 3311-1 Yakushiji, Shimotsuke-shi, Tochigi 329-0498, Japan)

  • Mitsuhiro Omine

    (Internal Medicine, Showa University Fujigaoka Hospital, 1-30 Fujigaoka, Aoba-ku, Yokohama, Kanagawa 227-8501, Japan)

  • Hisamaru Hirai

    (Cell Therapy and Transplantation Medicine, and,
    Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan)

  • Hiromitsu Nakauchi

    (Exploratory Research for Advanced Technology, Japan Science and Technology Agency, 4-1-8 Honcho, Kawaguchi-shi, Saitama 332-0012, Japan
    Center for Stem Cell and Regenerative Medicine)

  • H. Phillip Koeffler

    (Hematology/Oncology, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048, USA)

  • Seishi Ogawa

    (Cancer Genomics Project,
    Core Research for Evolutional Science and Technology,)

Abstract

Gain-of-function oncogenes Normal human cells contain a complete set of chromosomes from each parent, but in some cancers both copies of parts of particular chromosomes are from the same parent — a phenomenon known as acquired uniparental disomy. Work on genomic DNA from over 200 bone marrow samples from patients with myeloid neoplasms has uncovered a high incidence of inheritance of two copies of part of chromosome 11 from a single parent, containing a gain-of-function mutation of the tumour suppressor C-CBL that causes fibroblast cells to become cancerous and renders haematopoietic cells more sensitive to cytokine stimulation. The data support the idea that c-Cbl is both a growth-suppressing tumour suppressor gene and, when mutated, a growth-promoting oncogene, a situation similar to that found for the p53 tumour suppressor.

Suggested Citation

  • Masashi Sanada & Takahiro Suzuki & Lee-Yung Shih & Makoto Otsu & Motohiro Kato & Satoshi Yamazaki & Azusa Tamura & Hiroaki Honda & Mamiko Sakata-Yanagimoto & Keiki Kumano & Hideaki Oda & Tetsuya Yamag, 2009. "Gain-of-function of mutated C-CBL tumour suppressor in myeloid neoplasms," Nature, Nature, vol. 460(7257), pages 904-908, August.
    • Handle: RePEc:nat:nature:v:460:y:2009:i:7257:d:10.1038_nature08240
    DOI: 10.1038/nature08240
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