In a Turkish cohort, H. pylori-positive gastric cancer biopsies showed markedly reduced microbial diversity, near-absent Helicobacter (<0.01%), Firmicutes depletion, and Proteobacteria/Enterobacteriaceae (Morganella, Providencia, Klebsiella) enrichment, which the authors interpret as supporting the 'hit-and-run' model in which H. pylori initiates carcinogenesis but is outcompeted by a pro-inflammatory dysbiotic community.
Microbial alpha diversity (richness and evenness) was significantly reduced in the H. pylori-positive gastric cancer group compared with all other groups.
Overall microbial community structure (beta diversity) of the Hp+GC group diverged sharply from non-malignant controls.
The Hp+GC microbiota showed massive depletion of Firmicutes and overrepresentation of Proteobacteria.
Helicobacter relative abundance was dominant in non-malignant Hp+NUD samples but fell to negligible levels in gastric cancer biopsies despite clinical H. pylori positivity.
The Hp+GC niche was enriched with potentially pathogenic Enterobacteriaceae, specifically Morganella, Providencia, and Klebsiella.
The authors conclude the findings support the 'hit-and-run' model of H. pylori in gastric carcinogenesis.
This study examined the bacteria living in stomach tissue samples from 96 people in Turkey, comparing people with gastric cancer to those with non-ulcer dyspepsia (a milder, non-cancerous condition), both with and without Helicobacter pylori infection. The researchers sequenced bacterial DNA from 158 biopsies to see which microbes were present. In people with gastric cancer who were clinically positive for H. pylori, the stomach bacterial community was much less diverse than in the other groups. H. pylori itself was almost undetectable in their cancer biopsies (<0.01%), while it was the dominant bacterium in non-cancer patients with H. pylori. Instead, the cancer samples were dominated by other bacteria, particularly gut-associated Enterobacteriaceae such as Morganella, Providencia, and Klebsiella, and Proteobacteria made up about two-thirds of the community. The authors interpret this as supporting a 'hit-and-run' idea: H. pylori may start the process leading to cancer, then be displaced by other bacteria as the stomach lining becomes damaged and less acidic. This research suggests that stomach bacteria beyond H. pylori may matter in gastric cancer, but this was a cross-sectional comparison in a modest-sized group, so it cannot by itself show that these bacteria cause cancer or that the sequence of events happens as proposed.
Kocazeybek B, Bal K, Akkus S, Demirci M, Kurt E, Gareayaghi N, et al.. (2026). Association of Gastric Microbiota with Gastric Cancer in Patients Infected with Helicobacter pylori.. Pathogens (Basel, Switzerland). https://doi.org/10.3390/pathogens15101051