BCR-ABL与Src家族激酶相互作用介导CML对抗癌药物伊马替尼耐受的研究进展  

Progress of the BCR-ABL and Src family kinases interactions leading CML to imatinib-resistance

作　　者：王冠明[1] 林晨[1] 陈小华[1] 李扬秋[2] 

机构地区：[1]暨南大学医学院微生物与免疫学系,广州510632 [2]暨南大学血液研究所,广州510632

出　　处：《生命科学》2013年第1期47-53,共7页Chinese Bulletin of Life Sciences

基　　金：广州市科技支撑计划项目(2009Z1-E161);广东省自然科学基金项目(06025169)

摘　　要：BCR/ABL融合蛋白是慢性粒细胞白血病(CML)的分子标志,具有高激酶活性,其在疾病发生、发展中扮演了极其重要的角色。伊马替尼(Imatinib)靶向抑制BCR-ABL,为CML慢性期的一线治疗药。BCR/ABL与Src家族激酶(Src-family kinases,SFK)之间也存在相互活化作用,通过激活众多信号通路,导致CML向急变期发展,并导致伊马替尼耐药。对有关BCR/ABL与SFK两者的相互作用机制及其生物学效应的研究进行总结。BCR-ABL fusion protein is the molecular marker of chronic myeloid leukemia （CML）, which has constitutive kinase activity, playing an essential role in the pathogenesis of CML. Imatinib specially inhibits BCR- ABL, which is considered as the frontline treatment in the chronic phase of CML（CP-CML）. Studies have shown that the interaction between BCR-ABL fusion protein and Src family kinases induces the activation of multiple signaling pathways which are responsible for the transition from CP to BP of CML and induction of imatinib resistance. In this paper, we reviewed the progress of the BCR/ABL and Src family kinases interaction machanisms and their biological effects.

关 键 词：慢性粒细胞白血病 BCR—ABL Src家族激酶 伊马替尼耐药 

分 类 号：Q555.7[生物学—生物化学] R733.72[医药卫生—肿瘤]