期刊
CELL CYCLE
卷 9, 期 6, 页码 1051-1056出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.9.6.11034
关键词
c-CBL; 11qUPD; myeloproliferative neoplasms; gain-of-function; MDS/MPN; tyrosine kinases
类别
资金
- NCI NIH HHS [R01 CA026038, R01 CA026038-30A2, R01 CA026038-31, R01 CA026038-32] Funding Source: Medline
C-CBL (CBL) encodes a multifunctional protein engaged in the regulation of intracellular signaling pathways.(1,2) It was first identified as a cellular counterpart of the viral oncogene, v-CBL, that causes murine lymphoma.(3,4) 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.(5-9) In this review, we summarize our current knowledge about c-CBL mutations and discuss the molecular mechanisms of their gain-of-function.
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