Language

English

Publication Date

1-1-2026

Journal

Clinical and Experimental Gastroenterology

DOI

10.2147/CEG.S495588

PMID

41531650

PMCID

PMC12983157

PubMedCentral® Posted Date

1-7-2026

PubMedCentral® Full Text Version

Post-print

Abstract

Helicobacter pylori (H. pylori) is a human bacterial pathogen that causes one of the most common chronic bacterial infections worldwide. The microorganism has been classified by the International Agency for Research on Cancer as a Group I carcinogen. While the etiological link to gastric cancer is well established, the precise molecular and cellular mechanisms driving this transformation are highly complex and incompletely understood. Fundamentally, the infection results from the chronic presence of acute on chronic gastric mucosal inflammation. H. pylori pathogenicity is increased by bacterial virulence factors including the cytotoxin-associated gene A (CagA) and Vacuolating cytotoxin A (VacA) which may interfere with the host’s cell communication and create a pro-tumorigenic microenvironment. Host microRNAs (miRNAs) may amplify these effects by modulating immune responses, enhancing oncogenic signalling. Despite the proven benefits of H. pylori eradication in reducing cancer risk, especially in high-incidence regions, rising antibiotic resistance and host-related variables impede its global implementation. Recent advances in genomics and multi-omics profiling potentially offer new opportunities for targeted prevention. Moreover, emerging evidence suggests H. pylori may also negatively influence immunotherapy outcomes, underscoring its broader relevance in cancer treatment planning. By synthesizing molecular insights, epidemiological trends, and clinical data, this narrative review examines the multifaceted pathways through which H. pylori contributes to gastric carcinogenesis, integrating current knowledge on microbial virulence, host signalling disruption, immune modulation, and epigenetic remodelling.

Keywords

Helicobacter pylori, gastric cancer, pathogenesis, CagA, VacA, virulence

Published Open-Access

yes

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