抑癌基因CpG岛甲基化与结直肠癌关系的研究进展  

CpG island methylation of tumor suppressor genes in colorectal cancer

作　　者：彭星宇[1] 曾庆黎[1] 

机构地区：[1]江西省人民医院普通外科,江西南昌330006

出　　处：《中国普通外科杂志》2012年第10期1279-1282,共4页China Journal of General Surgery

基　　金：江西省科技厅资助项目(2010BSA14200)

摘　　要：CpG岛甲基化可导致抑癌基因的表观遗传学转录失活,在某些情况下可能是抑癌基因失活的惟一机制,直接导致肿瘤的发生。笔者对Syk,p15,hMLHl,APC,DCC,p16等抑癌基因CpG岛甲基化与结直肠癌的关系进行简要综述,并提出存在的问题和展望。CpG island methylation can lead to epigenetic transcription inactivation of the tumor suppressor gene, and in some circumstances it may be the only mechanism of tumor suppressor gene inactivation, which directly results in the occurrence of the tumors. This paper overviews the relations of the CpG island methylation of the tumor suppressor gene such as Syk, and ofpl5 with colorectal cancer, and also presents related problems and future considerations.

关 键 词：结直肠肿瘤 抑癌基因 CPG岛 甲基化 综述文献 

分 类 号：R735.3[医药卫生—肿瘤]