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机构地区:[1]青岛大学医学院附属医院内镜诊治科,山东省青岛市266003 [2]青岛大学医学院附属医院临床医学研究所,山东省青岛市266003
出 处:《世界华人消化杂志》2010年第6期606-609,共4页World Chinese Journal of Digestology
摘 要:目的:探讨hMSH2基因启动子区5'CpG岛高甲基化在胃癌发生过程中的作用.方法:应用甲基化特异性PCR(methylation specific PCR,MSP)方法检测胃癌及非癌组织中hMSH2基因启动子区甲基化状态.结果:40例胃癌中hMSH2基因启动子区高甲基化24例(60%),其癌旁黏膜组织中有15例(37.5%)发生甲基化,14例慢性萎缩性胃炎组织中有5例(35.7%)发生甲基化,6例慢性浅表性胃炎组织中未见甲基化.四组甲基化水平相比,差别有统计意义(P<0.05).胃癌组甲基化水平高于癌旁组,差别有统计意义(P<0.05).癌旁组、慢性萎缩性胃炎组、慢性浅表性胃炎组三组甲基化水平相比,差别无统计意义.胃癌各临床病理参数组之间相比差别无统计意义.结论:胃癌组织中hMSH2基因启动子区高甲基化可能是导致其错配修复功能缺陷的重要原因之一;而错配修复功能缺陷在胃癌的发生中起着重要作用,但可能与其发展关系不大.AIM: To detect the role of methylation of the 5’ CpG island located in the promoter region of the human mutS homolog-2 (hMSH2) gene in the pathogenesis of gastric carcinoma. METHODS: The methylation of the hMSH2 promoter was examined by methylation-specific polymerase chain reaction (MSP) in 40 gastric carcinoma specimens, 40 matched cancer-adjacent mucosa specimens, 14 chronic atrophic gastritis (CAG) specimens, and 6 chronic superficial gastritis (CSG) specimens. RESULTS: The methylation of the hMSH2 promoter was detected in 24 out of the 40 (60%)gastric cancer specimens, 15 out of the 40 (37.5%) cancer-adjacent mucosa specimens, and 5 out of the 14 (35.7%) CAG specimens. No methylation was detected in 6 CSG specimens. The rate of hMSH2 promoter methylation was significantly higher in gastric cancer tissue than in non-carcinoma tissue (P 0.05). No significant differences were detected in the rates of hMSH2 promoter methylation among cancer-adjacent mucosa specimens, CAG specimens and CSG specimens. The rate of hMSH2 promoter methylation is not correlated with the clinicopathological parameters of gastric cancer. CONCLUSION: The hMSH2 promoter methylation may be a main mechanism responsible for mismatch repair (MMR) dysfunction that is involved in the development, but not the progression, of gastric cancer.
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