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河南林州地区贲门癌和癌旁组织中p16基因启动子甲基化及蛋白表达
引用本文:张梅,王立东,王俊宽,吴会芳,郭涛,冯笑山,李吉林,焦新英,李江曼,李寒冰,范宗民. 河南林州地区贲门癌和癌旁组织中p16基因启动子甲基化及蛋白表达[J]. 中华肿瘤防治杂志, 2007, 14(7): 494-496
作者姓名:张梅  王立东  王俊宽  吴会芳  郭涛  冯笑山  李吉林  焦新英  李江曼  李寒冰  范宗民
作者单位:河南省食管癌重点开放实验室,郑州大学医学实验中心癌症研究室,河南,郑州,450052;平顶山市第一人民医院,河南,平顶山,467000;河南省食管癌重点开放实验室,郑州大学医学实验中心癌症研究室,河南,郑州,450052;林州市姚村食管癌医院病理科,河南,林州,456592;平顶山市第一人民医院,河南,平顶山,467000
基金项目:国家自然科学基金;国家自然科学基金;河南省医学科技攻关项目;河南省高等学校杰出科研人才创新工程
摘    要:目的探讨贲门癌变过程中p16基因启动子区甲基化和p16蛋白表达变化特征和规律及其相互关系。方法采用甲基化特异PCR(MSP)及免疫组化方法,检测林州地区32例贲门癌患者癌组织、癌旁不典型增生组织和正常组织p16基因启动子区甲基化状态及蛋白表达情况。结果p16基因在癌组织中表达缺失18例(56%),不典型增生组织中表达缺失8例(73%);26例(81%)癌组织、7例(64%)不典型增生组织和18例(67%)正常组织发生了p16基因启动子区的甲基化。贲门癌组织中p16基因甲基化与表达缺失一致率为56%。差异无统计学意义,P〉0.05。结论p16蛋白表达缺失可能是贲门癌变过程中的重要分子事件,p16基因启动子区甲基化可能是导致其蛋白表达缺失的机制之一。

关 键 词:蛋白质p16/代谢  基因  p16  甲基化  胃肿瘤/遗传学  胃肿瘤/病理学  贲门
文章编号:1673-5269(2007)07-0494-03
收稿时间:2006-01-10
修稿时间:2007-03-20

Promoter hypermethylation and protein expression of p16 gene in gastric cardia adenocarcinoma and adjacent non-cancer tissues in Linzhou, Henan Province
ZHANG Mei,WANG Li-dong,WANG Jun-kuan,WU Hui-fang,GUO Tao,FENG Xiao-shan,LI Ji-lin,JIAO Xin-ying,LI Jiang-man,LI Han-bing,FAN Zong-min. Promoter hypermethylation and protein expression of p16 gene in gastric cardia adenocarcinoma and adjacent non-cancer tissues in Linzhou, Henan Province[J]. Chinese Journal of Cancer Prevention and Treatment, 2007, 14(7): 494-496
Authors:ZHANG Mei  WANG Li-dong  WANG Jun-kuan  WU Hui-fang  GUO Tao  FENG Xiao-shan  LI Ji-lin  JIAO Xin-ying  LI Jiang-man  LI Han-bing  FAN Zong-min
Abstract:OBJECTIVE: To characterize the p16 protein expression and promoter hypermethylation in gastric cardia carcinogenesis. METHODS: Immunohisto-chemistry and methylation specific PCR were used to detect p16 protien expression and p16 gene promoter methylation in adjacent non-cancer tissue, dysplasia tissue (DYS) and gastric cardia adenocarcinoma (GCA) from 32 patients with GCA, respectively. RESULTS: Aberrant expression rates of p16 protein were 18(56%) and 8(73%) in GCA and DYS tissues, respectively. The prevalence of p16 gene hypermethylation was 26(81%), 7(64%) and 18(67%) in GCA, DYS and normal tissues, respectively. The confordence rate of promotor methylation and expression dletion of p16 gene in GCA tissues was 56%, it did not have statistic difference in confordence, P>0.05. CONCLUSION: Aberrant expression of p16 is one of frequent molecular events in gastric cardia carcinogenesis and p16 hypermethylation may be one of mechanisms leading to p16 protein aberrant expression.
Keywords:gastric cardia adenocarcinoma    pl6 gene    hypermet hylation
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