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Interplay and cooperation of Helicobacter pylori and gut microbiota in gastric carcinogenesis.

Seyedeh Zahra Bakhti, +1 more
- 23 Sep 2021 - 
- Vol. 21, Iss: 1, pp 258-258
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TLDR
In this paper, a comprehensive overview of the effects of gut microbiota and H. pylori on the development of gastric cancer was provided, and the potential mechanisms of intestinal microbiota were discussed in gastric carcinogenesis.
Abstract
Chronic Helicobacter pylori infection is a critical risk factor for gastric cancer (GC). However, only 1–3 % of people with H. pylori develop GC. In gastric carcinogenesis, non-H. pylori bacteria in the stomach might interact with H. pylori. Bacterial dysbiosis in the stomach can strengthen gastric neoplasia development via generating tumor-promoting metabolites, DNA damaging, suppressing antitumor immunity, and activating oncogenic signaling pathways. Other bacterial species may generate short-chain fatty acids like butyrate that may inhibit carcinogenesis and inflammation in the human stomach. The present article aimed at providing a comprehensive overview of the effects of gut microbiota and H. pylori on the development of GC. Next, the potential mechanisms of intestinal microbiota were discussed in gastric carcinogenesis. We also disserted the complicated interactions between H. pylori, intestinal microbiota, and host in gastric carcinogenesis, thus helping us to design new strategies for preventing, diagnosing, and treating GC.

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References
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Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation

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Journal Article

Human Gastric Carcinogenesis: A Multistep and Multifactorial Process—First American Cancer Society Award Lecture on Cancer Epidemiology and Prevention

TL;DR: A human model of gastric carcinogenesis with the following sequential stages: chronic gastritis; atrophy; intestinal metaplasia; and dysplasia, which has been linked with the supply of beta-carotene and with excessive salt intake is provided.
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