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背景与目的:胃癌是一种多因素相关疾病,幽门螺杆菌(Helicobactorpylori,HP)感染是导致胃癌发生的原因之一,但其分子机制不明。错配修复基因是保证DNA复制高保真度的重要基因,与消化道肿瘤发生具有密切关系。本研究通过检测HP感染和非感染胃癌组织及癌旁粘膜组织和慢性浅表性胃炎粘膜组织中错配修复基因hMSH2和hMLH1蛋白的表达,探讨hMSH2、hMLH1基因在胃癌发生中的作用和HP致癌的可能机制。方法:采用尿素酶快速检验法对HP感染情况进行检测;利用免疫组化方法检测胃癌及癌旁粘膜和胃炎粘膜组织中hMSH2和hMLH1的表达情况,采用χ2检验对数据进行统计学分析。结果:hMSH2在胃癌组织中的阳性率(67.1%),显著高于癌旁粘膜组织(35.5%)和胃炎粘膜组织(42.1%)(P<0.05),而后两者无显著性差异(P>0.05)。癌组织中低分化腺癌的hMSH2阳性率(81.1%)显著高于高中分化腺癌(54.5%)和粘液癌(52.9%)(P<0.05);后两者间无显著性差异(P>0.05)。hMLH1的阳性率在胃癌组织(81.6%)、癌旁粘膜组织(90.8%)和胃炎组织(89.5%)间无显著性差异(P>0.05)。hMLH1在粘液癌中的阳性率(47.1%)显著低于高中分化腺癌(81.8%)和低分化腺癌(97.3%)(P<0.05),而后两者间无显著性差异(P>0.05)。在HP感染和非感染胃癌组织中,hMSH2的阳性率分别为56.8%和81.3%,
BACKGROUND & OBJECTIVE: Gastric cancer is a multifactorial disease. Helicobacter pylori (HP) infection is one of the causes of gastric cancer, but its molecular mechanism is unknown. Mismatch repair gene is an important gene to ensure the high fidelity of DNA replication, and is closely related to the occurrence of gastrointestinal tumors. This study was designed to investigate the role of hMSH2 and hMLH1 in gastric carcinogenesis and HP carcinogenesis by detecting the expression of mismatch repair genes hMSH2 and hMLH1 in HP-infected and non-infected gastric tissues, adjacent mucosa tissues and chronic superficial gastritis mucosa tissues Possible mechanism. Methods: HP infection was detected by urease rapid test. The expression of hMSH2 and hMLH1 in gastric mucosa and adjacent mucosa and gastritis mucosa were detected by immunohistochemistry. The data were analyzed by χ2 test. Results: The positive rate of hMSH2 in gastric cancer was 67.1%, which was significantly higher than that in adjacent mucosa (35.5%) and gastric mucosa (42.1%) (P <0.05), but there was no significant difference between them (P> 0.05). The positive rate of hMSH2 in poorly differentiated adenocarcinoma (81.1%) was significantly higher than that in high differentiated adenocarcinoma (54.5%) and mucinous carcinoma (52.9%) (P <0.05). There was no significant difference between the two groups (P> 0.05). The positive rate of hMLH1 was not significantly different between gastric cancer (81.6%), paracancer mucosa (90.8%) and gastritis (89.5%) (P> 0.05). The positive rate of hMLH1 in mucinous carcinoma (47.1%) was significantly lower than that in high differentiated adenocarcinoma (81.8%) and poorly differentiated adenocarcinoma (97.3%) (P <0.05), but there was no significant difference between them ). In HP infected and non-infected gastric cancer tissues, the positive rates of hMSH2 were 56.8% and 81.3%, respectively,