Ansari S, Ahmed N. Pathogenicity of Helicobacter pylori-associated gastric cancer. World J Clin Oncol 2025; 16(12): 110909 [DOI: 10.5306/wjco.v16.i12.110909]
Corresponding Author of This Article
Shamshul Ansari, PhD, Assistant Professor, Division of Health Sciences, Higher Colleges of Technology, Baniyas, Abu Dhabi 25026, United Arab Emirates. shamshulansari483@yahoo.com
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Oncology
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Review
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
Dec 24, 2025 (publication date) through Dec 29, 2025
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World Journal of Clinical Oncology
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2218-4333
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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
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Ansari S, Ahmed N. Pathogenicity of Helicobacter pylori-associated gastric cancer. World J Clin Oncol 2025; 16(12): 110909 [DOI: 10.5306/wjco.v16.i12.110909]
World J Clin Oncol. Dec 24, 2025; 16(12): 110909 Published online Dec 24, 2025. doi: 10.5306/wjco.v16.i12.110909
Pathogenicity of Helicobacter pylori-associated gastric cancer
Shamshul Ansari, Nada Ahmed
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. shamshulansari483@yahoo.com
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
Abstract
Gastric cancer (GC) is one of the leading causes of cancer-related deaths worldwide and ranks among the top five most common malignancies. Helicobacter pylori (H. pylori) infection is recognized as the primary risk factor, although gastric carcinogenesis also reflects complex interactions among bacterial virulence factors, host genetics, and the gastric microbiome. H. pylori harbors well-characterized proteins such as CagA, VacA, BabA, and SabA that enable persistent infection and fuel tumor initiation. Recent high-quality evidence from randomized trials and meta-analyses provide strong support that H. pylori eradication therapy substantially reduces cancer risk-even in those with established precancerous lesions such as intestinal metaplasia or dysplasia. Additionally, emerging research indicate that H. pylori may influence the tumor immune microenvironment, such as through altering programmed death ligand 1 expression-which could affect immunotherapy outcomes. This review presents a cohesive and updated perspective on H. pylori-driven GC, summarizing bacterial virulence, host predispositions, microbiome interactions, epigenetic changes like DNA repair gene methylation, and evolving therapeutic implications, all while illuminating current scientific debates and emerging directions
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.
