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. 2022 May 15;14(5):959–972. doi: 10.4251/wjgo.v14.i5.959

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©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.

-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/

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Possible mechanisms involved (A) in the etiology of non-cardiac gastric cancer (intestinal type) resulting in the classical cascade of Correa histopathological precancerous lesions (B) as seen in an upper gastrointestinal endoscopy. Hp-I: Helicobacter pylori infection; GC: Gastric cancer; PPIs: Proton pump inhibitors; CagA: Cytotoxin-associated gene A; VacA: Vacuolating cytotoxin A; GGT: γ-glutamyl transpeptidase; BabA: Blood-group-antigen-binding adhesin; SabA: Sialic acid-binding adhesin; OipA: Outer inflammatory protein; NapA: Neutrophil activation protein A; EMT: Epithelial-mesenchymal transition; ROS/RNS: Reactive oxygen species/Reactive nitrogen species; EGFR: Epidermal growth factor receptor; SPEM: Spasmolytic polypeptide-expressing metaplasia; CSC: Cancer stem cell; BMDSCs: Bone marrow-derived stem cells; IEN: Intraepithelial neoplasia.