Loading
Life sciences · Journal article
Frontiers in Immunology · September 14, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Gastric cancer remains a leading cause of cancer-related mortality worldwide. The classical Helicobacter pylori -centric paradigm of gastric carcinogenesis is being progressively expanded, as it is now recognized that the stomach harbors a complex and metabolically active microbial ecosystem whose compositional shifts fundamentally influence oncogenic progression. This review proposes a unifying dysbiosis-carcinogenesis-immune remodeling-therapeutic intervention (DCIT) framework to integrate the rapidly growing body of evidence linking gastric microbiota dysbiosis to malignancy. We survey the compositional landscape of the gastric microbiota across the Correa cascade, from healthy homeostasis through atrophic gastritis, intestinal metaplasia, and adenocarcinoma, and examine the ecological succession that releases niche constraints for oral commensals and nitrate-reducing taxa in advanced disease stages. We systematically evaluate four complementary mechanistic axes of microbial carcinogenesis: genotoxicity driven by bacterial effectors, chronic inflammation sustained by pattern recognition receptor signaling, epithelial barrier disruption facilitating bacterial translocation, and metabolic reprogramming of the gastric niche generating carcinogenic N -nitroso compounds and secondary bile acids. The review further examines how gastric microbiota remodels the tumor immune microenvironment through immune cell reprogramming, metabolite-mediated signaling, and checkpoint modulation, with direct implications for the efficacy of immune checkpoint inhibitor immunotherapy. The translational pipeline is evaluated from established H. pylori eradication regimens through probiotics, phage therapy, and fecal microbiota transplantation to emerging strategies that integrate microbiota modulation with chemotherapy and immunotherapy. Finally, we assess the methodological challenges of low-biomass gastric microbiome research, the integration of multi-omics platforms, and the critical evidence gaps that need to be addressed to realize the clinical potential of microbiota-targeted strategies for gastric cancer prevention and treatment.