Department of Internal Medicine, St. Vincent Hospital, The Catholic University of Korea, Suwon, Korea.
Korean J Gastroenterol. 2023 Oct 25;82(4):171-179. doi: 10.4166/kjg.2023.097.
Chronic inflammation due to a () infection is a representative cause of gastric cancer that can promote gastric carcinogenesis by abnormally activating immune cells and increasing the inflammatory cytokines levels. infections directly cause DNA double-strand breaks in gastric epithelial cells and genetic damage by increasing the enzymatic activity of cytidine deaminase. Eventually, gastric cancer is induced through dysplasia. Hypermethylation of tumor suppressor genes is an important cause of gastric cancer because of a infection. In addition, the changes in gastric microbiota and the mucosal inflammatory changes associated with a co-infection with the Epstein-Barr virus are associated with gastric cancer development. DNA damage induced by and the subsequent responses of gastric stem cells have implications for gastric carcinogenesis. Although the pathogenesis of H. pylori has been established, many uncertainties remain, requiring more study.
由 () 感染引起的慢性炎症是导致胃癌的一个代表性原因，它可以通过异常激活免疫细胞和增加炎症细胞因子水平来促进胃癌的发生。 感染通过增加胞嘧啶脱氨酶的酶活性，直接导致胃上皮细胞的 DNA 双链断裂和遗传损伤。最终，通过发育不良导致胃癌。由于 感染，肿瘤抑制基因的 hypermethylation 是胃癌的一个重要原因。此外，与 Epstein-Barr 病毒共同感染相关的胃微生物群变化和黏膜炎症变化也与胃癌的发展有关。 和随后的胃干细胞反应引起的 DNA 损伤与胃癌的发生有关。虽然已经确定了 H. pylori 的发病机制，但仍存在许多不确定性，需要进一步研究。
