Nguyen Thi Hong Chuyen, Nguyen Tran Bao Song, Nguyen Thanh Phuc, Ha Thi Minh Thi, Pham Nguyen Cuong, Nguyen Thi Thu Giang, Phan Minh Tri, Le Thanh Huy, Ha Thanh Thanh, Nguyen Tran Thuc Huan, Dang Cong Thuan
Department of Oncology, University of Medicine and Pharmacy, Hue University, Hue, Vietnam.
Department of Histology, Embryology, Pathology, and Forensic Medicine, University of Medicine and Pharmacy, Hue University, Hue, Vietnam.
Nagoya J Med Sci. 2025 Feb;87(1):93-104. doi: 10.18999/nagjms.87.1.93.
Gastric cancer is a common malignancy disease with a poor prognosis. Deficient mismatch repair is a prognostic and predictive marker of response to systemic therapies. However, deficient mismatch repair frequency and the relationship between this status and microscopic characteristics are inconsistent across nations. We aimed to determine the rate of deficient mismatch repair and its association with histopathological features in gastric cancer patients. A cross-sectional study was conducted on 226 gastric cancer patients treated at Hue University of Medicine and Pharmacy Hospital and Hue Central Hospital from June 2020 to January 2024. Mismatch repair protein expression was evaluated using immunohistochemical staining, and any absence of mismatch repair proteins was regarded as deficient mismatch repair. The deficient mismatch repair rate was 12.8%. Deficient mismatch repair appeared to be more frequent in the intestinal subtype of Lauren classification odds ratio (OR) = 4.767 (95% confidence interval [CI], 1.086-20.921; p = 0.039), tubular/papillary adenocarcinoma (OR = 5.25; 95% CI, 1.185-23.251; p = 0.029), mucinous adenocarcinoma (OR = 6.19; 95% CI, 1.113-34.445; p = 0.037), and differentiated type (OR = 3.24; 95% CI, 1.324-7.931; p = 0.01). No statistically significant association was detected with histopathological features according to the Tumor Location-Modified Lauren classification and mucinous secreting morphology. Deficient mismatch repair status was unusual in gastric cancer. The degree of cell differentiation and microscopic characteristics based on the World Health Organization and Lauren classification could all impact the predictive power for microsatellite-instable status.
胃癌是一种常见的恶性疾病,预后较差。错配修复缺陷是全身治疗反应的预后和预测标志物。然而,错配修复缺陷的频率以及这种状态与微观特征之间的关系在不同国家并不一致。我们旨在确定胃癌患者错配修复缺陷的发生率及其与组织病理学特征的关联。对2020年6月至2024年1月在顺化医科大学医院和顺化中心医院接受治疗的226例胃癌患者进行了一项横断面研究。使用免疫组织化学染色评估错配修复蛋白表达,任何错配修复蛋白的缺失都被视为错配修复缺陷。错配修复缺陷率为12.8%。在劳伦分类的肠型中,错配修复缺陷似乎更常见,优势比(OR)=4.767(95%置信区间[CI],1.086 - 20.921;p = 0.039),管状/乳头状腺癌(OR = 5.25;95%CI,1.185 - 23.251;p = 0.029),黏液腺癌(OR = 6.19;95%CI,1.113 - 34.445;p = 0.037),以及分化型(OR = 3.24;95%CI,1.324 - 7.931;p = 0.01)。根据肿瘤位置改良的劳伦分类和黏液分泌形态,未检测到与组织病理学特征有统计学意义的关联。错配修复缺陷状态在胃癌中并不常见。基于世界卫生组织和劳伦分类的细胞分化程度和微观特征都可能影响微卫星不稳定状态的预测能力。