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Prevalence and clinicopathological/molecular characteristics of mismatch repair protein-deficient tumours among surgically treated patients with prostate cancer in a Japanese hospital-based population.

日本医院人群中手术治疗的前列腺癌患者中错配修复蛋白缺陷型肿瘤的患病率和临床病理/分子特征。

  • 影响因子:2.04
  • DOI:10.1093/jjco/hyaa207
  • 作者列表:"Kagawa M","Kawakami S","Yamamoto A","Suzuki O","Eguchi H","Okazaki Y","Akagi K","Tamaru JI","Arai T","Yamaguchi T","Ishida H
  • 发表时间:2021-04-01
Abstract

BACKGROUND:The prevalence and molecular characteristics of deficient mismatch repair prostate cancer in the Japanese population have scarcely been investigated. METHODS:Immunohistochemistry for mismatch repair proteins (MLH1, MSH2, MSH6 and PMS2) was performed in formalin-fixed paraffin-embedded sections prepared from resected primary prostate cancers in patients who underwent prostatectomy at our institution between January 2001 and May 2016. Genetic and/or epigenetic alterations of mismatch repair genes were investigated in patients with any loss of mismatch repair protein expression in the tumour. RESULTS:Of the 337 patients, four (1.2%) showed loss of mismatch repair protein expression on immunohistochemistry. All four patients showed loss of both MSH2 and MSH6 protein expression. Genetic testing was performed in two of the four patients, demonstrating no pathogenic germline alterations were present. In each of these two patients, at least one somatic alteration inactivating MSH2 without MSH2 hypermethylation was identified, leading to the diagnosis of supposed 'Lynch-like syndrome'. Patients with deficient mismatch repair prostate cancer were at a significantly higher stage (pT2pN0 vs. pT3-4pN0/pTanypN1, P = 0.02) and had a greater Gleason score (<8 vs. ≥8, P < 0.01) than those with proficient mismatch repair prostate cancer. CONCLUSIONS:The prevalence of deficient mismatch repair prostate cancer in the Japanese hospital-based prostatectomized population was extremely low. To improve screening efficacy for deficient mismatch repair prostate cancer, screening candidates can be limited to patients with locally advanced, node-positive and/or Gleason score of 8 or greater prostate cancer. Universal tumour screening for Lynch syndrome seems ineffective in patients with prostate cancer.

摘要

背景: 在日本人群中,缺乏错配修复前列腺癌的患病率和分子特征鲜有研究。 方法: 在2001年1月至2016年5月在我们机构接受前列腺切除术的患者中,在福尔马林固定的石蜡包埋切片中进行错配修复蛋白 (MLH1、MSH2、MSH6和PMS2) 的免疫组织化学。在肿瘤中错配修复蛋白表达任何缺失的患者中研究错配修复基因的遗传和/或表观遗传改变。 结果: 337例患者中,4例 (1.2%) 免疫组化显示错配修复蛋白表达缺失。所有4例患者均显示MSH2和MSH6蛋白表达缺失。对4名患者中的2名进行了基因检测,证明不存在致病性种系改变。在这两名患者中,至少有一个体细胞改变使MSH2失活而没有MSH2高甲基化,这导致了所谓的 “林奇样综合征” 的诊断.错配修复缺陷前列腺癌患者的分期 (pT2pN0 vs. pT3-4pN0/pTanypN1,P = 0.02) 显著高于错配修复前列腺癌患者 (pT2pN0 vs./pTanypN1,P = 0.01),且Gleason评分 (<8 vs. ≥ 8,P <) 高于错配修复前列腺癌患者。 结论: 在日本医院前列腺切除人群中,错配修复缺陷型前列腺癌的患病率极低。为了改善缺陷错配修复前列腺癌的筛查功效,筛查候选者可以限于具有局部晚期、淋巴结阳性和/或Gleason评分为8或更高的前列腺癌的患者。Lynch综合征的通用肿瘤筛查在前列腺癌患者中似乎无效。

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影响因子:2.68
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DOI:10.1007/s11033-021-06299-9
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