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作 者:魏国华[1] 杨春雨[1] 杨静[1] 李辉[1] 高志安
机构地区:[1]辽宁医学院病理学教研室,辽宁锦州121000
出 处:《中国现代医学杂志》2010年第10期1490-1493,共4页China Journal of Modern Medicine
基 金:辽宁省自然科学基金(002073)
摘 要:目的探讨p16基因异常甲基化在胃癌发生中的作用。方法应用甲基化特异性PCR技术检测胃腺癌及癌前病变组织中p16基因甲基化状态,并应用免疫组化染色检测p16蛋白的表达。结果慢性萎缩性胃炎、重度异型增生及胃腺癌组织p16基因启动子甲基化阳性率分别为11.1%、40%和43.3%。胃腺癌组与浅表性胃炎组、萎缩性胃炎组及轻-中度异型增生组间p16基因甲基化阳性率差异有显著性(P<0.05),而与重度异型增生组间差异无显著性(P>0.05)。p16蛋白阳性率在胃腺癌组、重度异型增生、轻-中度异型增生、萎缩性胃炎组和浅表性胃炎组分别为36.7%、40%、85.7%、83.3%和100%;在19例p16基因甲基化阳性病例中,18例p16蛋白缺失。结论 p16基因启动子异常甲基化可能是其在胃癌蛋白表达缺失的主要原因。p16基因启动子异常甲基化可能是胃癌发生的早期事件,在胃癌的发生起重要作用。[Objective]To investigate the effect of aberrant methylation of p16 gene in the pathogenesis of gastric carcinoma.[Methods]Hypermethylation of p16 promoter region were detected by MSP in 30 cases of gastric carcinoma ,18 cases of chronic atrophic gastritis,17 cases of gastric dysplasia and 10 cases of chronic superficial gastritis . Expression of p16 protein was assessed by immunohistochemistry.[Results]In the groups of chronic atrophic gastritis, severe dysplasia and gastric carcinoma, aberrant promoter methylation of p16 gene was obtained 11.1%, 40% and 43.3% ,respectively, no p16 gene promoter methylation was detected in the groups of light-moderate dysplasia and chronic superficial gastritis. Significant statistically differences were obtained among the groups of carcinoma and chronic atrophic gastritis, light-moderate dysplasia and chronic superficial gastritis, but no significant statistically difference was detected between the groups of severe dysplasia and adenocarcinoma. In the groups of chronic atrophic gastritis, gastric dysplasia, light-moderate dysplasia, severe dysplasia and gastric carcinoma , p16 protein expression were observed 100%,83.3%,85.7%,40%,36.7%,respectively. In 19 cases of p16 gene methylation, p16 protein negative expression were observed in 18 cases[.Conclusion]Aberrant methylation of p16 promoter region may contribute to the lack of p16 protein in gastric carcinoma. Aberrant promoter methylation of p16 gene may be an early event and play an important role in the pathogenesis of gastric adenocarcinoma.
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