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目的探讨子宫内膜非典型增生中错配修复基因(mismatch repair gene,MMR)蛋白MLH1、MSH2、PMS2和MSH6的表达,微卫星不稳定性及意义。方法应用免疫组织化学法检测DNA错配修复蛋白MLH1、PMS2、MSH2和MSH6在子宫内膜非典型增生(50例)及正常增生期宫内膜组织(50例)中的表达,分析微卫星不稳定性与子宫内膜非典型增生临床特征的关系。结果 50例子宫内膜非典型增生组织中MLH1、MSH2、PMS2、MSH6失表达率分别为12%(6/50)、14%(7/50)、12%(6/50)和8%(4/50);MLH1、PMS2、MSH6的表达率高于正常增生期子宫内膜,差异具有统计学意义(P<0.05),两组MSH2的表达差异无统计学意义(P=0.338)。以蛋白失表达情况分组,子宫内膜非典型增生组MSI-H表型7例(14%),MSI-L表型9例(18%),MSS表型34例(68%),与正常增生期宫内膜组比较,差异具有统计学意义(P=0.005)。在子宫内膜非典型增生中,年龄≤50岁者MSI-H明显高于>50岁者(P=0.001)。结论 MMR系蛋白失表达及MSI可能是子宫内膜非典型增生重要分子事件之一。
Objective To investigate the expression and microsatellite instability of mismatch repair gene (MMR) MLH1, MSH2, PMS2 and MSH6 in atypical hyperplasia of endometrium. Methods The expression of DNA mismatch repair proteins MLH1, PMS2, MSH2 and MSH6 in endometrial dysplasia (50 cases) and normal endometrial tissues (50 cases) were detected by immunohistochemistry. Relationship between stability and clinical features of atypical atypical hyperplasia. Results The loss rates of MLH1, MSH2, PMS2 and MSH6 in 50 cases of endometrial dysplasia were 12% (6/50), 14% (7/50), 12% (6/50) and 8% 4/50). The expression rates of MLH1, PMS2 and MSH6 were higher than those in normal proliferative endometrium (P <0.05). There was no significant difference in the expression of MSH2 between the two groups (P = 0.338). The MSI-H phenotype was found in 7 cases (14%), MSI-L phenotype in 9 cases (18%), and MSS phenotype in 34 cases (68%) in the group of endometrial dysplasia, The difference was statistically significant (P = 0.005). In atypical hyperplasia of the endometrium, MSI-H was significantly higher in patients ≤50 years of age than> 50 years (P = 0.001). Conclusion The loss of MMR expression and MSI may be one of the important molecular events of atypical hyperplasia of endometrium.