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    Cell Cycle. 2010 Mar 15;9(6):1051-6. Epub 2010 Mar 15.

    Gain-of-function c-CBL mutations associated with uniparental disomy of 11q in myeloid neoplasms.

    Ogawa S, Sanada M, Shih LY, Suzuki T, Otsu M, Nakauchi H, Koeffler HP.

    Source

    Cancer Genomics Project, University of Tokyo, Bunkyo-ku, Tokyo, Japan. sogawa-tky@umin.ac.jp

    Abstract

    c-CBL (CBL) encodes a multifunctional protein engaged in the regulation of intracellular signaling pathways. It was first identified as a cellular counterpart of the viral oncogene, v-CBL, that causes murine lymphoma. Although no genetic evidence existed suggesting its role in human carcinogenesis, the recent discovery of c-CBL mutations in myeloid cancers has unveiled a unique oncogenic mechanism mediated by gain-of-function of a mutated tumor suppressor, closely associated with allelic conversion of 11q arms. In this review, we summarize our current knowledge about c-CBL mutations and discuss the molecular mechanisms of their gain-of-function.

    PMID:
    20237427
    [PubMed - indexed for MEDLINE]
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