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

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 Yamagata, Junko Takita, Noriko Gotoh, Kumi Nakazaki, Norihiko Kawamata, Masafumi Onodera, Masaharu Nobuyoshi, Yasuhide Hayashi, Hiroshi Harada, Mineo Kurokawa, Shigeru Chiba, Hiraku Mori, Keiya Ozawa, Mitsuhiro Omine, Hisamaru Hirai, Hiromitsu Nakauchi, H. Phillip Koeffler and Seishi Ogawa ()
Additional contact information
Masashi Sanada: Cancer Genomics Project,
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,
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,
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,
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,
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,
Hiromitsu Nakauchi: Exploratory Research for Advanced Technology, Japan Science and Technology Agency, 4-1-8 Honcho, Kawaguchi-shi, Saitama 332-0012, Japan
H. Phillip Koeffler: Hematology/Oncology, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048, USA
Seishi Ogawa: Cancer Genomics Project,

Nature, 2009, vol. 460, issue 7257, 904-908

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.

Date: 2009
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DOI: 10.1038/nature08240

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