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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 HPCell Cycle 2010[Mar]; 9 (6): 1051-6c-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.|Animals[MESH]|Bone Marrow Neoplasms/*genetics[MESH]|Chromosomes, Human, Pair 11/*genetics[MESH]|Humans[MESH]|Mutation/*genetics[MESH]|Myeloproliferative Disorders/*genetics[MESH]|Proto-Oncogene Proteins c-cbl/*genetics[MESH]|Uniparental Disomy/*genetics[MESH] |
