Gut Microbiota as Potential Biomarker and/or Therapeutic Target to Improve the Management of Cancer Original paper

What was reviewed?

This review evaluated how gut microbiota patterns can function as cancer biomarkers and therapeutic targets, then concentrated on colibactin-producing, pks-positive Escherichia coli as a clinically relevant microbial feature in colorectal cancer. The authors synthesized human cohort data on fecal and mucosa-associated microbial signatures for screening and prognosis, and they integrated mechanistic work explaining how specific bacteria influence tumor biology and treatment response. Within that framework, they treated colibactin-producing E. coli as a prime example of a pathobiont that links microbial colonization to measurable molecular injury and clinically meaningful outcomes.

Who was reviewed?

The paper drew evidence from observational studies in people with colorectal cancer and controls using stool, mucosal, tissue, and occasionally blood-based microbial readouts, alongside preclinical validation in multiple mouse models and cell-based systems. For the colibactin focus, the review relied heavily on studies comparing mucosa-associated pks-positive E. coli in colorectal cancer tissue versus noncancer tissue, plus experimental models where colonization with colibactin-producing strains altered tumor development, immune context, or therapy response. It also discussed broader cancer settings, including cohorts that linked baseline gut microbiota profiles to immunotherapy outcomes in non-CRC cancers.

What were the most important findings?

The review emphasized that no single “universal” colorectal cancer microbiome exists, but reproducible patterns emerge that include enrichment of Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis, and colibactin-associated pks-positive E. coli, especially when organisms are detected near the mucosa. For microbiome-signature databases, the major microbial association that stands out is mucosa-associated CoPEC because it ties a taxonomic feature to a defined genotoxic mechanism. The authors highlighted converging evidence that colibactin can alkylate DNA, generate cross-links and double-strand breaks, create AT-rich damage hotspots, and leave recognizable mutational footprints that appear in subsets of human colorectal tumors. They also underscored non–DNA-only effects, including oxidative stress with impaired repair signaling, senescence with a growth-factor secretory program, and immune shaping characterized by reduced antitumor T-cell infiltration, which collectively support a tumor-promoting microenvironment.

What are the greatest implications of this study/ review?

This review supports using gut microbiota features as practical tools to improve cancer management, but it argues that the highest clinical value comes from biomarkers anchored to mechanism and proximity, such as pks-positive E. coli at the mucosa rather than stool-only presence. It also frames CoPEC as both a risk and progression marker and as a therapeutic target, suggesting that selectively blocking colibactin activity could reduce tumor-promoting pressure without needing broad microbiome eradication. Finally, it reinforces that microbiome-informed care must account for tumor heterogeneity and treatment context because bacteria can influence screening signals, prognosis, and therapy response through distinct pathways that may require different intervention strategies.