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子宫内膜癌错配修复蛋白表达的临床病理分析 被引量:15

Expression of DNA mismatch repair protein in endometrial carcinomas and its correlation with clinicopathologic features
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摘要 目的探讨错配修复蛋白表达缺失相关子宫内膜癌的临床病理特征。方法收集2014年12月至2015年8月间150例子宫内膜癌连续病例,收集临床病史,复阅病理切片并分析组织学类型、肿瘤内淋巴细胞浸润(≥42/10HPF)、肿瘤周围淋巴细胞浸润带、肿瘤异质性等特征。采用免疫组织化学法检测MLH1、MSH2、MSH6和PMS2蛋白,并分析错配修复蛋白表达状态与临床病理参数的相关性。结果错配修复蛋白表达缺失43例(28.7%),其中MLH1/PMS2配对表达缺失27例(18%),MSH2/MSH6配对表达缺失7例(4.7%)。MSH6单独表达缺失6例(4%),PMS2单独表达缺失3例(2%)。50岁以下及50岁以上子宫内膜癌患者错配修复蛋白表达缺失率分别为23.3%和27.1%,差异无统计学意义。12例具有家族肿瘤史患者中,错配修复蛋白表达缺失患者中,其年龄〈50岁的比例(4/6)明显高于错配修复蛋白正常表达患者(P=0.014)。错配修复蛋白表达缺失与肿瘤内淋巴细胞浸润(P=0.033)、显著的肿瘤周围淋巴细胞浸润带(P〈0.001)2项病理特征相关,也与浸润深度〈1/2肌层(P=0.039)及合并其他部位恶性肿瘤(卵巢透明细胞癌2例,肠癌1例;P=0.0322)相关。但与病变位于子宫体下段、肿瘤异质性、组织学类型、子宫内膜样腺癌分级、淋巴结有无转移、临床分期等均无明显相关性。结论肿瘤内淋巴细胞浸润增多、显著的肿瘤周围淋巴细胞浸润带是错配修复蛋白缺失子宫内膜癌相对特征性的病理形态,应引起病理医师的重视。错配修复蛋白表达缺失无明显年龄相关性,但在有相关肿瘤家族史患者中小于50岁者多见。 Objective To study the expression of mismatch repair protein in a series of endometrial carcinomas and its correlation with clinicopathologic features. Methods The clinical data of 150 consecutive cases of endometrial carcinoma were collected during the period from December, 2014 to August, 2015 in Fudan University Cancer Center. Morphologic features including tumor infiltrating lymphocytes (TIL), peritumoral lymphocytes and tumor heterogeneity were reviewed. Immunohistochemistry for expression of mismatch repair proteins was performed. The correlation with clinicopathologic features was analyzed. Results Loss of mismatch repair protein expression was observed in 43 cases (28.7%), including loss of MLH1/PMS2 in 27 cases ( 18% ), loss of MSH2/MSH6 in 7 cases (4.7%), loss of MSH6 in 6 cases (4%) and loss of PMS2 in 3 cases (2%). There were 23.3% and 27. 1% of mismatch repair protein-deficient endometrial carcinomas in women under and above 50 years of age, respectively, which was not statistically significant. Amongst the 12 cases with family history of tumors, 4 of the 6 mismatch repair protein-deficient cases were under 50 years of age, which was higher than that in the 6 cases with mismatch repair protein expression (P = 0. 014). The mismatch repair protein-deficient group showed significantly more prominent TIL and peritumoral lymphocytes than protein-expression group (P =0. 033 and 〈0. 001 ). Moreover, there were also significant differences in depth of myometrial invasion and occurrence of synchronous malignancy (2 cases of ovarian clear cell carcinoma and 1 case of colonic carcinoma) between the two groups ( P = 0. 039 and 0. 022). However, there were no significant differences in lymph node metastasis, tumor heterogeneity, lower uterine segment involvement and tumor stage between the two groups. Conclusions Prominent TIL and peritumoral lymphocytes characteristically occur in mismatch repair protein-deficient endometrial carcinomas. Patient age does not significantly correlate with the loss of mismatch repair protein expression, but individuals under 50 years of age are more likely to have no expression if there is family history of tumors.
出处 《中华病理学杂志》 CAS CSCD 北大核心 2016年第5期302-307,共6页 Chinese Journal of Pathology
关键词 子宫内膜肿瘤 DNA错配修复 结直肠肿瘤 遗传性非息肉性 病理学 临床 免疫组织化学 Endometrial neoplasms DNA mismatch repair Colorectal neoplasms, hereditary nonpolyposis Pathology, clinical Immunohistochemistry
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