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Helicobacter pylori is a well-established driver of gastric cancer (GC). However, emerging evidence highlights the oral-gastric axis as a previously underappreciated frontier in gastric carcinogenesis. In this review, we comprehensively summarize how oral microbiota dysbiosis may promote GC initiation and progression. Current literature indicates that oral pathobionts frequently translocate to the gastric niche. These microbes may contribute to tumorigenesis by sustaining chronic mucosal inflammation. They also potentially modulate tumor immune evasion and may promote cellular metabolic reprogramming. Furthermore, specific oral taxa exhibit profound synergistic crosstalk with H. pylori . This microbial synergy exacerbates the hostile tumor microenvironment and accelerates malignant transformation. Unraveling these multi-level regulatory networks underscores the immense clinical translational value of the oral-gastric axis. Specifically, oral microbial signatures offer great promise as non-invasive biomarkers for early diagnostic screening. They concurrently represent novel targets for precision microecological therapies. Finally, we identify critical knowledge gaps to guide future rigorous investigations in this rapidly evolving field.
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Tao et al. (2026) studied this question.
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