The relationship between the gut microbiome and cancer risk has moved well beyond correlation — emerging evidence now suggests that specific patterns of microbial imbalance may actively drive the development and progression of gastrointestinal cancers, while simultaneously offering tractable targets for intervention. This matters because colorectal, gastric, and hepatic cancers collectively account for a disproportionate share of global cancer mortality, and conventional screening and treatment approaches remain limited.
This review, published in Acta Pharmacologica Sinica, maps characteristic dysbiosis signatures across major gastrointestinal cancers, identifying microbial taxa whose enrichment or depletion correlates with tumor initiation, immune evasion, and metastatic potential. The analysis covers mechanistic pathways through which gut bacteria modulate the tumor microenvironment — including bile acid metabolism, short-chain fatty acid production, and inflammatory cytokine signaling — and surveys therapeutic strategies ranging from fecal microbiota transplantation and probiotic administration to phage-based bacterial depletion and microbiome-informed immunotherapy enhancement.
Positioning this work within the broader research landscape, microbiome-cancer research has accelerated substantially since the mid-2010s, when Fusobacterium nucleatum was implicated in colorectal cancer progression. This review represents a consolidation moment in a fast-moving field — synthesizing mechanistic, translational, and clinical data into a coherent framework. The practical implications are meaningful but must be tempered by key limitations: most mechanistic evidence remains preclinical, causal directionality between dysbiosis and cancer initiation is difficult to establish in humans, and microbiome composition is highly individualized, complicating generalizable therapeutic protocols. The field also lacks standardized dysbiosis diagnostic criteria. As a comprehensive review rather than original trial data, its strength lies in synthesizing existing evidence and identifying priority gaps. For health-conscious adults, it reinforces the plausibility — though not yet the clinical certainty — that long-term dietary patterns shaping microbial ecology may carry oncological consequences.
