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作 者:张友才[1] 陈金霞[1] 陈永平[1] 邓长生[2]
机构地区:[1]温州医学院附属第一医院,浙江温州325005 [2]武汉大学中南医院
出 处:《山东医药》2007年第10期16-17,共2页Shandong Medical Journal
基 金:湖北省科技攻关计划(2002AA301C84)
摘 要:目的探讨上皮型钙黏素(E-cad)基因启动子CpG岛甲基化与胃腺癌(GAC)和大肠腺癌(CRAC)的关系及意义。方法用甲基化特异性PCR技术检测82例GAC组织(GAC组)、30例十二指肠球部溃疡胃窦黏膜组织(对照组)、30例慢性胃炎伴肠上皮化生或异型增生胃黏膜组织(胃炎组)、94例CRAC组织(CARC组)及其癌旁非肿瘤组织中的E-cad基因启动子CpG岛甲基化状况。结果GAC组E-cad甲基化率显著高于对照组和胃炎组(P<0.01,<0.05),低分化者显著高于高、中分化者(P<0.05),~期肿瘤显著高于~期(P<0.05);CRAC组显著高于癌旁非肿瘤组织(P<0.01)。结论E-cad基因启动子CpG岛甲基化可能参与胃肠腺癌发生。[Objective] To study the relationship between promoter CpG islands methylation of E-cadherin (E-cad) and gastric adenocarcinoma (GAC),colorectal adenocarcinoma(CRAC). [Methods] Using methytationspecial PCR, we studied the methylation status of E-cad gene,promoter CpG islands of eighty-two GAC tumor tissues (GAC group), 30 duodenal ulcer gastric antral mucous tissues (control group),30 chronic gastritis mucous tissues with intestinal metaplasia or dysplasia(gatritis group), 94 CRAC tumor tissues (CRAC group) and its corresponding non-tumor tissues. [Results] The rate of E-cad gene CpG islands methylation in GAC Group was significantly higher than that of control group and gastritis group (P〈0.01, 〈0.05) ,in poorly differentiated patients was significantly higher than that of high or moderately differentiated patients (P〈0. 05),in stage Ⅲ- Ⅳ cases was significantly higher than that in stage Ⅰ -Ⅱ cases (P〈0. 05) ,in tumor tissues of CRAC was significantly higher than that of corresponding non-tumor tissues (P〈0.01). [Conclusion] CpG islands methylation of E-cad gene may be involved in the pathogenesis of GAC and CRAC.
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