ArticleCellular and molecular gastroenterology and hepatology2026
Helicobacter pylori-Induced Inflammatory Cancer Transformation Microenvironment Drives Gastric Carcinogenesis.
Article in Cellular and molecular gastroenterology and hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Rethinking Oxidative Stress inLife (Basel, Switzerland) · 2026Review
- Pan-immune-inflammation value is a novel prognostic biomarker in pT2-4 gastric cancer.Frontiers in medicine · 2026Article
- Gastric Cancer-Associated Immunomodulatory Fibroblasts Persist Following Helicobacter pylori Eradication: The Need to Douse a Smoldering Fire.Cellular and molecular gastroenterology and hepatology · 2026Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsHelicobacter pylori (H pylori) eradication significantly reduces gastric cancer risk but offers limited benefit for patients with advanced atrophic gastritis. After eradication, a persistent inflammatory-cancer-transformation microenvironment (ICTM) drives gastric carcinogenesis, warranting further investigation.
methodsWe constructed a single-cell atlas of 22 gastric antral mucosae across disease stages, including normal controls, H pylori-infected non-atrophic gastritis, H pylori-infected chronic atrophic gastritis, and post-eradication chronic atrophic gastritis (stratified by pathological improvement). Key findings were validated via multiplex immunofluorescence and primary cancer-associated fibroblast (CAF) experiments.
resultsH pylori infection profoundly alters the ICTM within immune and stromal cells during and after eradication. Following eradication, epithelial cells exhibit distinct trajectories after eradication, with the pathological improvement group showing increased MUC5AC expression and the non-improvement group displaying a malignant trajectory. Immunomodulatory CAFs (iCAFs) critically promote epithelial malignancy and immunosuppression. CCN2
conclusionsH pylori infection induces persistent ICTM after eradication. Infection-driven iCAF differentiation contributes to epithelial malignant transformation and a potential immunosuppressive microenvironment, linking to gastric carcinogenesis. Our findings underscore the critical role of ICTM transformation, highlighting the need to improve ICTM for post-H pylori eradication therapies, and indicate that specific iCAF subtypes represent promising intervention targets.
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