FHIT基因及其与食管癌关系的研究进展  

Progress in the relationship of fragile histidine triad gene and esophageal cancers

作　　者：刘建昆[1] 周曾芬[2] 范宗江[1] 

机构地区：[1]成都军区昆明总医院消化内科,650032 [2]昆明医学院第一附属医院消化内科,650032

出　　处：《国际消化病杂志》2006年第3期192-194,共3页International Journal of Digestive Diseases

摘　　要：FHIT基因定位于3p14．2,研究证实其为一押癌基因。其失活机制主要表现为缺失、异常转录本以及启动子区城CpG岛甲基化,其抑癌作用可能与诱导细胞凋亡、细胞周期阻滞及二腺苷三磷酸水解酶、微管蛋白、泛素结合酶等有关。FHIT基因在食管癌中早期即有频繁缺失及异常表达,提示FHIT基因在食管癌发生发展中可能起关键作用。The Fragile Histidine Trind （FHIT） is a tumor suppressor gene at chromosome 3p14.2 that has identified by positional cloning . The mechanisms for inactivating the gene have been revealed to deletions , aderrant transcripts and methylation of the 5′CpG-island. The tumor suppressor effect is probably related with inducing cell apoptosis, cell cycle retardation , diadenosine 5′,5＂-pl ,p3 triphosphate hydrolase, tubulin and ubiquitin conjugase. FHIT gene deletion and abnormal expression in early stage esophageal carcinoma suggest that FHIT may play a key role in the carcinogenesis and progression of human esophageal cancers.

关 键 词：FHIT 抑癌基因 食管肿瘤 

分 类 号：R735.1[医药卫生—肿瘤]