早期胃癌内镜下黏膜剥离术及幽门螺杆菌根除后异时性胃癌的发生机制研究进展  

Research progress on the mechanism of metachronous gastric cancer after endoscopic submucosal dissection and Helicobacter pylori eradication in early gastric cancer

作　　者：胡馨月 王斌 王涛 刘凯军 文良志 陈东风 Hu Xin-Yue;Wang Bin;Wang Tao;Liu Kai-Jun;Wen Liang-Zhi;Chen Dong-Feng(Department of Gastroenterology,Army Medical Center,Army Medical University,Chongqing 400042,China)

机构地区：[1]陆军军医大学陆军特色医学中心消化内科,重庆400042

出　　处：《解放军医学杂志》2024年第1期108-114,共7页Medical Journal of Chinese People's Liberation Army

基　　金：国家重点研发计划(2022YFA1105302)。

摘　　要：幽门螺杆菌(HP)感染是胃癌的Ⅰ类致癌因子,与胃癌的发生密切相关。众多研究表明根除HP对胃癌有预防作用,但早期胃癌行内镜下黏膜剥离术(ESD)后根除HP仍有2.7%~6.1%的患者可发生异时性胃癌(MGC),其发生机制尚不清楚。本文从HP根除后胃黏膜萎缩及肠化生不能完全逆转、胃黏膜上皮细胞过度增殖及遗传异常累积、表观组稳态失衡、免疫微环境变化、胃黏膜干细胞异常、染色质可及性、染色体重塑改变等角度,阐述早期胃癌行ESD及HP根除后上述分子改变导致癌变的机制。Helicobacter pylori(HP)infection is a ClassⅠcarcinogen in gastric cancer,closely related to the occurrence of gastric cancer.Many studies have shown that HP eradication has a preventive effect on gastric cancer.However,2.7%-6.1%of patients with early gastric cancer who have been eradicated after endoscopic submucosal dissection(ESD)can still develop metachronous gastric cancer(MGC),and the mechanism of its occurrence is still unclear.In this review,the atrophy of gastric mucosa and intestinal metaplasia cannot be completely reversed after HP eradication,the excessive proliferation of gastric mucosa epithelial cells,the accumulation of genetic abnormalities,the homeostasis imbalance of the epigenetic group,changes in immune microenvironment,the abnormality of stem cells in gastric mucosa,chromatin accessibility,and changes in chromosome remodeling were discussed in the mechanism of carcinogenesis caused by the above molecular changes after ESD and HP eradication in early gastric cancer.

关 键 词：胃黏膜剥离术 幽门螺杆菌 根除治疗 异时性胃癌 发生机制 

分 类 号：R735.2[医药卫生—肿瘤]