Research progress on the mechanism of metachronous gastric cancer after endoscopic submucosal dissection and Helicobacter pylori eradication in early gastric cancer
10.11855/j.issn.0577-7402.0460.2023.0719
- VernacularTitle: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
- Author:
Xin-Yue HU
1
;
Bin WANG
;
Tao WANG
;
Kai-Jun LIU
;
Liang-Zhi WEN
;
Dong-Feng CHEN
Author Information
1. 陆军军医大学陆军特色医学中心消化内科,重庆 400042
- Keywords:
endoscopic submucosal dissection;
Helicobacter pylori;
eradication;
metachronous gastric cancer;
pathogenesis
- From:
Medical Journal of Chinese People's Liberation Army
2024;49(1):108-114
- CountryChina
- Language:Chinese
-
Abstract:
Helicobacter pylori(HP)infection is a Class Ⅰ carcinogen 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.
