食管癌发生的分子生物学机制  

Molecular biology mechanism of esophageal carcinogenesis

作　　者：邹磊[1] 王荣华[2] 李道堂[1] 

机构地区：[1]山东省肿瘤医院胸外科,山东济南250117 [2]章丘市人民医院胸心外科,山东章丘250200

出　　处：《中华肿瘤防治杂志》2006年第5期388-390,共3页Chinese Journal of Cancer Prevention and Treatment

摘　　要：食管癌癌变的发生发展机制是一个涉及多因素、多阶段、多基因变异积累及相互作用的复杂过程,这个过程可能发生在基因组DNA水平上,也可能在mRNA或蛋白质水平上。近年来对食管癌发生机制的分子生物学研究提示,该过程呈多阶段演变,并伴有多基因的交互及叠加作用,特别是癌基因的激活和抑癌基因的失活,是导致细胞异常增殖并进而发生癌变的重要基础。细胞周期调控、信号传导、细胞分化、损伤修复及凋亡等方面的分子生物学机制是导致肿瘤发生和发展不可或缺的因素。对于食管癌发生的分子生物学机制的探讨将有助于阐明其癌变机制,确立癌变过程的重要分子靶点,从而为肿瘤的基因诊断和治疗提供思路。With regard to its cancerization mechanism has not been discovered yet. Most published studies indicate that it is a complex procedure involved in multiple factor, multiple stage and polygenic variation. The procedure takes place possibly on the level of genome DNA, mRNA or protein. In recent years esophageal cancer molecular bioresearch suggest that this process appears to multiple stage evolution, accompanying with polygenic reciprocation and additive effect. Oncogene activation and anti-oncogene inactivation are thought to be the important foundation that lead to cell abnormal proliferation with the result that cancerization. Molecular biology mechanisms including cell cycle regulation, signal conduction, cell differentiation, lesion repair and apoptosis are indispensable factors leading to tumorigenesis and growth. Research on the molecular biology mechanism of esophageal carcinogenesis help＇s to illuminate cancerization mechanism and establish pronusing molecule target, thus,offer directions for tumorous gene diagnosis and therapy.

关 键 词：食管肿瘤 分子生物学 综述文献 

分 类 号：R735.1[医药卫生—肿瘤]