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上尿路尿路上皮癌:与错配修复蛋白缺失及林奇综合征的关联频率

Upper tract urothelial carcinomas: frequency of association with mismatch repair protein loss and lynch syndrome.

作者信息

Harper Holly L, McKenney Jesse K, Heald Brandie, Stephenson Andrew, Campbell Steven C, Plesec Thomas, Magi-Galluzzi Cristina

机构信息

Robert J. Tomsich Pathology and Laboratory Medicine Institute, Cleveland Clinic, Cleveland, OH, USA.

Glickman Urological Institute, Cleveland Clinic, Cleveland, OH, USA.

出版信息

Mod Pathol. 2017 Jan;30(1):146-156. doi: 10.1038/modpathol.2016.171. Epub 2016 Oct 7.

Abstract

Increased risk for upper tract urothelial carcinoma is described in patients with Lynch syndrome, caused by germline mutations in mismatch repair genes. We aimed to identify the frequency of mismatch repair protein loss in upper tract urothelial carcinoma and its potential for identifying an association with Lynch syndrome. We queried our database to identify upper tract urothelial carcinomas. Patients were cross-referenced for history of colorectal carcinoma or other common Lynch syndrome-associated neoplasms to enrich for potential Lynch syndrome cases. Tumor histopathologic characteristics were reviewed and each case was analyzed for loss of mismatch repair proteins, MLH1, MSH2, MSH6, and PMS2, by immunohistochemistry. Of 444 patients with upper tract urothelial carcinoma, a subset of 215 (encompassing 30 with upper tract urothelial carcinoma and another common Lynch syndrome-associated neoplasm) was analyzed for loss of mismatch repair protein expression. Of 30 patients with Lynch syndrome-associated neoplasms, six had documented Lynch syndrome, including two with Muir-Torre syndrome. Mismatch repair protein loss was identified in 7% of total upper tract urothelial carcinomas and 30% of patients with Lynch syndrome-associated neoplasms (including all patients with Lynch syndrome/Muir-Torre syndrome). Of patients without history of Lynch syndrome-associated neoplasms, 5 of 184 (2.7%) had loss of mismatch repair protein expression. Twelve cases with mismatch repair protein loss demonstrated loss of MSH2 and MSH6, and 2 had isolated loss of MSH6. MLH1 and PMS2 expression were consistently retained. Although increased intratumoral lymphocytes, inverted growth, pushing tumor-stromal interface, and lack of nuclear pleomorphism were more commonly seen in cases with mismatch repair protein loss, only intratumoral lymphocytes and presence of pushing borders were statistically significant. MLH1 and PMS2 testing appear to have little utility in upper tract urothelial carcinoma; however, mismatch repair protein loss of MSH2 and/or MSH6 by immunohistochemistry seems relatively sensitive and specific for identifying patients with potential Lynch syndrome.

摘要

林奇综合征患者发生上尿路尿路上皮癌的风险增加,该综合征由错配修复基因的种系突变引起。我们旨在确定上尿路尿路上皮癌中错配修复蛋白缺失的频率及其识别与林奇综合征相关性的潜力。我们查询数据库以识别上尿路尿路上皮癌。对患者进行结肠直肠癌或其他常见林奇综合征相关肿瘤病史的交叉对照,以富集潜在的林奇综合征病例。回顾肿瘤组织病理学特征,并通过免疫组织化学分析每个病例错配修复蛋白MLH1、MSH2、MSH6和PMS2的缺失情况。在444例上尿路尿路上皮癌患者中,对215例患者(包括30例上尿路尿路上皮癌合并另一种常见林奇综合征相关肿瘤的患者)进行了错配修复蛋白表达缺失分析。在30例林奇综合征相关肿瘤患者中,6例有记录的林奇综合征,包括2例穆尔-托雷综合征患者。在上尿路尿路上皮癌总数的7%以及林奇综合征相关肿瘤患者的30%(包括所有林奇综合征/穆尔-托雷综合征患者)中发现了错配修复蛋白缺失。在无林奇综合征相关肿瘤病史的患者中,184例中有5例(2.7%)有错配修复蛋白表达缺失。12例错配修复蛋白缺失的病例显示MSH2和MSH6缺失,2例仅有MSH6缺失。MLH1和PMS2表达始终保留。虽然错配修复蛋白缺失的病例中更常见肿瘤内淋巴细胞增多、倒置生长、推挤肿瘤-间质界面和缺乏核多形性,但只有肿瘤内淋巴细胞和推挤边界的存在具有统计学意义。MLH1和PMS2检测在上尿路尿路上皮癌中似乎效用不大;然而,通过免疫组织化学检测MSH2和/或MSH6的错配修复蛋白缺失似乎对识别潜在林奇综合征患者相对敏感且特异。

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