Digestion · 2026
Gastric Cancer in the Post-<italic>Helicobacter pylori</italic> Era: Non-<italic>H</italic>. <italic>pylori</italic>-Related Gastric Microbiota, Non-<italic>H</italic>. <italic>pylori-</italic>Related and Post-<italic>H. pylori</italic> Eradication Gastric Cancer.
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Tan Andrew Xia Huang, Tee Nicholas Chin Hock, Ang Tiing Leong
Аннотация
BACKGROUND: Helicobacter pylori-negative gastric cancer (GC) occurs in individuals with specific risk factors. This narrative review will evaluate the role of non-H. pylori gastric microbiota in gastric carcinogenesis and summarize the clinical aspects of non-H. pylori-related GC.
SUMMARY: Epstein-Barr virus is the only other infection conclusively proven to be causative of GC. Case-control studies have reported a dysbiotic GC-associated gastric microbiome, with greater abundance of Fusobacterium nucleatum, Streptococcus anginosus, Prevotella, and Veillonella. Mice model mechanistic studies have demonstrated the role of non-H. pylori microbiota in gastric carcinogenesis. Current data support their role as promotive factors, with H. pylori infection being the initiating event. In hereditary GC, inherited germline mutations initiate a genetically programmed pathway to gastric carcinogenesis. Autoimmune atrophic gastritis and Ménétrier's disease are associated with increased GC risk. Oxyntic gland adenoma/gastric adenocarcinoma of fundic gland type and foveolar-type gastric adenoma are distinct histological subtypes of gastric neoplasia. Chronic atrophic gastritis (CAG) and gastric intestinal metaplasia (GIM) persist even after H. pylori eradication, increasing GC risk.
KEY MESSAGES: There must be greater awareness of H pylori-negative GC as a diagnostic possibility due to the impact on management. There is significant potential for translational application of gastric microbiome as predictive or prognostic biomarkers or even to shape treatment outcomes. Endoscopic surveillance is indicated in the case of extensive CAG or GIM, even after successful H. pylori eradication.
SUMMARY: Epstein-Barr virus is the only other infection conclusively proven to be causative of GC. Case-control studies have reported a dysbiotic GC-associated gastric microbiome, with greater abundance of Fusobacterium nucleatum, Streptococcus anginosus, Prevotella, and Veillonella. Mice model mechanistic studies have demonstrated the role of non-H. pylori microbiota in gastric carcinogenesis. Current data support their role as promotive factors, with H. pylori infection being the initiating event. In hereditary GC, inherited germline mutations initiate a genetically programmed pathway to gastric carcinogenesis. Autoimmune atrophic gastritis and Ménétrier's disease are associated with increased GC risk. Oxyntic gland adenoma/gastric adenocarcinoma of fundic gland type and foveolar-type gastric adenoma are distinct histological subtypes of gastric neoplasia. Chronic atrophic gastritis (CAG) and gastric intestinal metaplasia (GIM) persist even after H. pylori eradication, increasing GC risk.
KEY MESSAGES: There must be greater awareness of H pylori-negative GC as a diagnostic possibility due to the impact on management. There is significant potential for translational application of gastric microbiome as predictive or prognostic biomarkers or even to shape treatment outcomes. Endoscopic surveillance is indicated in the case of extensive CAG or GIM, even after successful H. pylori eradication.