Gastric Microbiome Dynamics in Cancer Pathogenesis

The stomach hosts a complex ecosystem of microorganisms whose composition and function shift markedly during the progression from healthy mucosa through precancerous lesions to overt malignancy. While Helicobacter pylori remains a principal initiator of chronic gastritis and atrophic changes, emerging evidence reveals that other bacterial taxa, including oral commensals and anaerobes, colonise the altered gastric niche, driving inflammation, barrier disruption and genotoxicity. Dysbiotic communities can modulate local immune surveillance, favouring tumour-promoting inflammation and evasion of cytotoxic T-cell responses. Metabolic cross-talk between microbes and epithelial cells generates nitrosating agents, short-chain fatty acids and other metabolites that influence cell proliferation, apoptosis and stromal remodelling. Integration of multi-omics approaches has begun to unravel the mechanistic axes by which specific bacteria adhere to epithelial receptors, activate mitogen-activated pathways and reshape the tumour immune microenvironment. Such insights underpin the development of microbial biomarkers for early detection, risk stratification and personalised immunotherapy, and suggest that targeted modulation of the gastric microbiome may complement existing preventive and therapeutic strategies worldwide.

Research from Nature Portfolio

Detailed community profiling first established that gastric carcinoma is characterised by a marked reduction in overall microbial diversity and a shift away from Helicobacter-dominance towards enrichment of intestinal commensals and oral-associated genera. A dysbiosis index combining key taxa discriminates carcinoma from non-malignant gastritis with high accuracy and reveals increased nitrosating potential in cancerous tissues. Subsequent analyses demonstrated that patients with gastric cancer frequently harbour Clostridium and Fusobacterium species at elevated abundance, forming a cancer-specific signature distinct from non-cancer controls. These foundational studies illuminate how loss of acid-mediated microbial control and overgrowth of pro-inflammatory anaerobes contribute to carcinogenesis and may serve as diagnostic or prognostic indicators.

Gastric Microbiome Dynamics in Cancer Pathogenesis publication trend

The graph below shows the total number of articles in gastric microbiome dynamics in cancer pathogenesis across all publications each year (not limited to Nature Index journals).

Technical terms

Gastric microbiome: The community of bacteria, archaea, viruses and fungi residing in the stomach lining.

Dysbiosis: A deleterious imbalance in microbial composition that disrupts host homeostasis.

Metagenomics: Culture-independent sequencing of collective microbial genomes.

Mitogen-activated protein kinase (MAPK) pathway: A signalling cascade regulating cell growth, differentiation and survival.

Tumour immune microenvironment: The local assemblage of immune cells, stroma and signalling molecules surrounding tumour cells.

Atrophy: Reduction in size or function of gastric glands, often preceding metaplasia.

Metaplasia: Reversible transformation of one differentiated cell type to another, associated with increased cancer risk.

References

1. Streptococcus anginosus promotes gastric inflammation, atrophy, and tumorigenesis in mice. Cell (2024).
2. Unveiling the gastric microbiota: implications for gastric carcinogenesis, immune responses, and clinical prospects. Journal of Experimental & Clinical Cancer Research (2024).
3. Characterization of the landscape of the intratumoral microbiota reveals that Streptococcus anginosus increases the risk of gastric cancer initiation and progression. Cell Discovery (2024).
4. Gastric microbial community profiling reveals a dysbiotic cancer-associated microbiota. Gut (2017).
5. Increased Abundance of Clostridium and Fusobacterium in Gastric Microbiota of Patients with Gastric Cancer in Taiwan. Scientific Reports (2018).
6. Dysbiosis of the microbiome in gastric carcinogenesis. Scientific Reports (2017).