Helicobacter pylori-associated Chronic Atrophic Gastritis and Progression of Gastric Carcinogenesis.

Na Rae Lim, Woo Chul Chung
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引用次数: 0

Abstract

Chronic inflammation due to a Helicobacter pylori (H. pylori) infection is a representative cause of gastric cancer that can promote gastric carcinogenesis by abnormally activating immune cells and increasing the inflammatory cytokines levels. H. pylori 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 H. pylori 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 H. pylori 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.

幽门螺杆菌相关的慢性萎缩性胃炎与胃癌的进展。
幽门螺杆菌(H.pylori)感染引起的慢性炎症是癌症的一个代表性原因,它可以通过异常激活免疫细胞和增加炎性细胞因子水平来促进胃癌的发生。幽门螺杆菌感染通过增加胞苷脱氨酶的酶活性,直接导致胃上皮细胞DNA双链断裂和遗传损伤。最后,癌症是通过发育不良诱发的。由于幽门螺杆菌感染,肿瘤抑制基因的高甲基化是癌症的重要原因。此外,胃微生物群的变化和与EB病毒共同感染相关的粘膜炎症变化与癌症的发展有关。幽门螺杆菌诱导的DNA损伤和随后胃干细胞的反应与胃癌的发生有关。尽管幽门螺杆菌的发病机制已经确定,但仍存在许多不确定性,需要更多的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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