[1]王 露,陈思敏,赵苏苏,等.子宫内膜样子宫内膜癌中错配修复基因表达与临床病理及相关基因表达的关系[J].医学信息,2020,33(14):61-66.[doi:10.3969/j.issn.1006-1959.2020.14.019]
 WANG Lu,CHEN Si-min,ZHAO Su-su,et al.Relationship Between Mismatch Repair Gene Expression and Clinicopathology and Related Gene Expression in Endometrioid Endometrial Carcinoma[J].Medical Information,2020,33(14):61-66.[doi:10.3969/j.issn.1006-1959.2020.14.019]
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子宫内膜样子宫内膜癌中错配修复基因表达与临床病理及相关基因表达的关系()
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医学信息[ISSN:1006-1959/CN:61-1278/R]

卷:
33卷
期数:
2020年14期
页码:
61-66
栏目:
论著
出版日期:
2020-07-15

文章信息/Info

Title:
Relationship Between Mismatch Repair Gene Expression and Clinicopathology and Related Gene Expression in Endometrioid Endometrial Carcinoma
文章编号:
1006-1959(2020)14-0061-06
作者:
王 露陈思敏赵苏苏
(江苏省中医院病理科,江苏 南京 210000)
Author(s):
WANG LuCHEN Si-minZHAO Su-suet al
(Department of Pathology,Jiangsu Provincial Traditional Chinese Medicine Hospital,Nanjing 210000,Jiangsu,China)
关键词:
子宫内膜样子宫内膜癌错配修复基因ERPRKi-67p16p53
Keywords:
Endometrioid endometrial carcinomaMismatch repair genesERPRKi-67p16p53
分类号:
R737.33
DOI:
10.3969/j.issn.1006-1959.2020.14.019
文献标志码:
A
摘要:
目的 分析错配修复(MMR)基因(MLH1、PMS2、MSH2、MSH6)的表达与子宫内膜样子宫内膜癌临床病理及ER、PR、p53、Ki-67、p16蛋白免疫组化表达的关系,探讨MMR基因及其他基因对子宫内膜样子宫内膜癌发生发展的作用。方法 收集2016年8月~2019年10月我院诊治的53例子宫内膜样腺癌患者的临床病理资料,应用免疫组织化学法检测癌组织中MLH1、PMS2、MSH2、MSH6、ER、PR、Ki-67、p16、p53的表达水平,分析癌组织中MLH1、PMS2、MSH2、MSH6的表达及其与临床病理、ER、PR、p53、Ki-67、p16表达的关系。结果 ①53例癌组织样本中MLH1、PMS2、MSH2、MSH6发生缺失表达的模式中,MLH1/PMS2缺失、MSH2/MSH6正常表达者最常见,其次是MSH2/MSH6缺失、MLH1/PMS2正常表达者, MLH1/PMS2/ MSH2/MSH6四个基因全部缺失表达仅1例;②MLH1/PMS2缺失、MSH2/MSH6正常表达者癌组织呈中分化者较多,而MMR基因全部正常表达者癌组织呈低分化者较多,差异有统计学意义(P<0.05);MSH2/MSH6缺失、MLH1/PMS2正常表达者肿块相对较大,p16表达呈阳性者相对较多,差异有统计学意义(P<0.05);MLH1/PMS2/ MSH2/MSH6四个基因全部缺失表达者的癌组织为低分化,ER、PR均阴性表达。结论 发生MMR蛋白缺失的子宫内膜样子宫内膜癌癌组织中,MLH1/PMS2缺失表达及MSH2/MSH6正常表达者最常见,MLH1/PMS2缺失表达及MSH2/MSH6正常表达的患者癌组织多为中分化,MSH2/MSH6缺失、MLH1/PMS2正常表达的患者肿块相对较大,p16表达呈阳性者较多。
Abstract:
Objective To analyze the relationship between the expression of mismatch repair (MMR) genes (MLH1, PMS2, MSH2, MSH6) and clinicopathology of endometrioid endometrial cancer and immunohistochemical expression of ER, PR, p53, Ki-67, p16 proteins to explore the role of MMR genes and other genes in the development of endometrioid endometrial cancer.Methods The clinical and pathological data of 53 patients with endometrioid adenocarcinoma diagnosed and treated in our hospital from August 2016 to October 2019 were collected. Immunohistochemistry was used to detect MLH1, PMS2, MSH2, MSH6, ER, PR, Ki-67, p16, p53 expression levels, analysis of MLH1, PMS2, MSH2, MSH6 expression in cancer tissues and its relationship with clinicopathology, ER, PR, p53, Ki-67, p16 expression.Results ①Among the 53 cancer tissue samples, MLH1, PMS2, MSH2, and MSH6 were found to be expressed in the missing pattern. MLH1/PMS2 deletion and MSH2/MSH6 normal expression were the most common, followed by MSH2/MSH6 deletion, MLH1/PMS2 normal expression,only one case of MLH1/PMS2/MSH2/MSH6 all four genes were deleted and expressed;②MLH1/PMS2 deletion, MSH2/MSH6 normal expression cancer tissues were more differentiated, and all MMR gene normal expression cancer tissues were poorly differentiated, the difference was statistically significant (P<0.05); MSH2/MSH6 those with deletion and normal expression of MLH1/PMS2 are relatively large, and those with positive expression of p16 are relatively large, the difference was statistically significant (P<0.05); cancer tissues of those with all four genes lacking expression of MLH1/PMS2/MSH2/MSH6 For poor differentiation, ER and PR are negatively expressed.Conclusion Among endometrioid endometrial carcinoma tissues with MMR protein deletion, MLH1/PMS2 deletion expression and MSH2/MSH6 normal expression are the most common. Patients with MLH1/PMS2 deletion expression and MSH2/MSH6 normal expression are mostly in patients with moderate differentiation, MSH2/MSH6 deletion, and normal expression of MLH1/PMS2, the tumor mass is relatively large, and p16 expression is positive.

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更新日期/Last Update: 1900-01-01