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目的探讨错配修复蛋白h MLH1、h MSH2和h MSH6在散发性结直肠癌(SCRC)中的表达情况及其与SCRC临床病理参数之间的关系。方法选取空军总医院普通外科和北京大学肿瘤医院结直肠外科2008年3月至2012年3月期间收治的SCRC患者263例,所有病例均经组织学证实且术前均未接受放化疗。采用免疫组织化学SP法检测263例SCRC患者肿瘤组织中h MLH1、h MSH2、h MSH6蛋白表达缺失情况,并分析其表达缺失与患者临床病理参数的关系。结果 263例SCRC患者肿瘤组织中h MLH1蛋白表达缺失率为13.3%(35/263),h MSH2蛋白表达缺失率为12.2%(32/263),h MSH6蛋白表达缺失率为28.9%(76/263),h MLH1/h MSH2表达共同缺失率为3.4%(9/263),h MLH1/h MSH6表达共同缺失率为10.2%(27/263),h MSH2/h MSH6表达共同缺失率为6.8%(18/263),h MLH1/h MSH2/h MSH6表达共同缺失率为3.4%(9/263)。h MSH1蛋白表达缺失率在高分化腺癌组织中明显高于中分化腺癌和低分化、黏液腺癌(P<0.01);h MSH2蛋白表达缺失率在直径>5 cm的肿瘤组织中明显高于直径≤5 cm的肿瘤组织(P<0.05);h MSH6蛋白表达缺失率在男性患者中明显高于女性患者(P<0.01),且在淋巴结转移少的肿瘤组织中明显高于淋巴结转移较多的肿瘤组织(P<0.01)。结论 h MLH1、h MSH2、h MSH6在SCRC中的表达缺失并不少见,且其表达缺失与SCRC患者临床病理参数的关系也明显不同于林奇综合征。因此,h MLH1、h MSH2、h MSH6在SCRC发生、发展中的作用可能也有别于林奇综合征。
Objective To investigate the expression of mismatch repair proteins h MLH1, h MSH2 and h MSH6 in sporadic colorectal cancer (SCRC) and their relationship with the clinicopathological parameters of SCRC. Methods Totally 263 SCRC patients admitted to the General Surgery Department of General Hospital of Air Force General Hospital and Department of Colorectal Surgery of Cancer Hospital of Peking University from March 2008 to March 2012 were enrolled in this study. All cases were confirmed by histology and did not receive radiochemotherapy before operation. Immunohistochemical SP method was used to detect the loss of hMLH1, h MSH2, h MSH6 protein in 263 cases of SCRC. The relationship between the expression of hMLH1, hMSH6 and clinicopathological parameters was analyzed. Results The loss of hMLH1 protein expression was 13.3% (35/263) in 263 cases of SCRC, 12.2% (32/263) cases in h hMSH2 protein and 28.9% 263). The common deletion rate of hMLH1 / h MSH2 expression was 3.4% (9/263), h MLH1 / h MSH6 expression common deletion rate was 10.2% (27/263), h MSH2 / h MSH6 expression common deletion rate was 6.8 % (18/263), h MLH1 / h MSH2 / h MSH6 expression was 3.4% (9/263). h The loss of MSH1 protein in well-differentiated adenocarcinoma was significantly higher than that in moderate-differentiated adenocarcinoma and poorly-differentiated adenocarcinoma (P <0.01). The loss of MSH2 protein was significantly higher in tumors> 5 cm in diameter (P <0.05). The loss of h MSH6 protein expression in male patients was significantly higher than that in female patients (P <0.01), and was significantly higher in lymph node metastasis than in lymph node metastasis More tumor tissue (P <0.01). Conclusion h MLH1, h MSH2, h MSH6 in SCRC expression loss is not uncommon, and its expression loss and SCRC patients with clinicopathological parameters also significantly different from Lynch syndrome. Therefore, h MLH1, h MSH2, h MSH6 in the occurrence of SCRC, the role of development may also be different from Lynch syndrome.