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©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Oncol. Dec 24, 2025; 16(12): 110909
Published online Dec 24, 2025. doi: 10.5306/wjco.v16.i12.110909
Published online Dec 24, 2025. doi: 10.5306/wjco.v16.i12.110909
Pathogenicity of Helicobacter pylori-associated gastric cancer
Shamshul Ansari, Division of Health Sciences, Higher Colleges of Technology, Abu Dhabi 25026, United Arab Emirates
Nada Ahmed, Microbiology and Immunology, Suez Canal University, Ismailia 41511, Al Ismailia, Egypt
Nada Ahmed, Division of Health Science, Higher Colleges of Technology, Abu Dhabi 25026, United Arab Emirates
Author contributions: Ansari S conceived and conceptualized the design of the study, reviewed and edited the manuscript; Ansari S and Ahmed N searched the published literature, extracted the core information and prepared the initial draft of the manuscript, revised the draft of the final manuscript.
Conflict-of-interest statement: The authors have no conflicts of interest to declare.
Open 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/
Corresponding author: Shamshul Ansari, PhD, Assistant Professor, Division of Health Sciences, Higher Colleges of Technology, Baniyas, Abu Dhabi 25026, United Arab Emirates.
Received: June 18, 2025
Revised: August 1, 2025
Accepted: November 13, 2025
Published online: December 24, 2025
Processing time: 188 Days and 11.5 Hours
Revised: August 1, 2025
Accepted: November 13, 2025
Published online: December 24, 2025
Processing time: 188 Days and 11.5 Hours
Core Tip
Core Tip: The factors beyond the well-known bacterial toxins, CagA and VacA, influence disease progression. Helicobacter pylori infection can cause DNA double-strand breaks and create a hypoxic environment in the stomach lining. This activates hypoxia-inducible factors, which promote processes like tissue remodeling, new blood vessel formation, and the appearance of cancer stem cell-like populations. At the same time, infection-driven changes in regulatory molecules such as microRNAs and long non-coding RNAs can silence tumor-suppressor genes and disrupt immune control. Together, these emerging factors amplify the damage initiated by bacterial virulence factors, accelerating the transformation of normal gastric cells into cancerous ones.