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作 者:张蕾[1] 邢德印[1] 谭文[1] 何祖根[1] 林东昕[1]
机构地区:[1]中国医学科学院中国协和医科大学肿瘤研究所肿瘤医院,北京100021
出 处:《癌症》2001年第12期1335-1338,共4页Chinese Journal of Cancer
基 金:"九五"国家医学重点科技攻关项目(No.96-906-01-06);国家杰出青年科学基金项目(No.39825122)
摘 要:目的:O6-甲基鸟嘌呤DNA甲基转移酶(MGMT)可以转移DNA加合物O6-甲基鸟嘌呤中的甲基,从而修复DNA损伤,许多肿瘤中发现MGMT基因启动子过甲基化导致该基因失活,我们研究了MGMT基因启动子甲基化状态与食管癌的关系。方法:采用甲基化特异性聚合酶链反应及测序方法分析食管癌、癌旁组织和正常食管上皮中MGMT启动子甲基化状态。结果:在检测的119例食管癌组织中,46例(38.7%)有MGMT基因启动子过甲基化;相应癌旁组织22例中也有5例(22.7%)出现MGMT基因甲基化,而21例正常食管上皮均无此种改变。结论:MGMT基因启动子过甲基化是食管癌中常见的分子事件,可能发生在癌变过程的早期阶段。Objective:O6 methylguanine DNA methyl transferase (MGMT) removes the methyl group from DNA adduct O6 methylguanine then to repair the damage.The MGMT gene has been shown to be silenced by promoter methylation in many human tumors.This study was designed to examine the relationship between the promoter methylation of the MGMT gene and esophageal squamous cell carcinoma.Methods:The promoter methylation of the MGMT gene was detected by methylation specific PCR in esophageal carcinoma tissues,tissues adjacent to the tumors, and normal esophageal mucosa. Results:Among the 119 esophageal carcinomas,MGMT hypermethylation was detected in 46 cases(38.7%). In the 22 tissues adjacent to the tumors,5 (22.7%) was found to have this epigenetic alteration. All the 21 normal tissues were shown to be unmethylated.Conclusion:Hypermethylation of the MGMT promoter is a frequent molecular event in esophageal cancer and may be involved in carcinogenesis at the early stage.
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