Microbial metabolomics and carcinogenesis: mechanistic pathways, clinical implications and methodological challenges
This narrative review maps associations between microbial metabolites and carcinogenesis but establishes no causality and provides no clinical intervention evidence.
| Outcome | Grade | Direction | Effect | Studies |
|---|---|---|---|---|
| Mechanistic pathways of carcinogenesis mediated by microbial metabolites | D | — Insufficient | narrativo, sem quantificação | — |
| Conversion of primary to secondary bile acids by the bacterial bai operon | C | ▲ Favorable | 6 enzimas necessárias/suficientes; sem IC | 1 |
| Microbial carcinogenesis biomarkers (identification) | D | — Insufficient | sem quantificação | — |
| Tumor microenvironment modulation by SCFAs | D | — Insufficient | narrativo, sem quantificação | — |
| Applicability of LC-MS and NMR in oncological microbial metabolomics | D | — Insufficient | descritivo, sem comparação quantitativa | — |
Context
Microbiome-derived metabolites (SCFAs, secondary bile acids, polyamines, amino acids) modulate inflammation, DNA integrity and the tumor microenvironment. These pathways are relevant to translational oncology. The absence of controlled clinical trials limits immediate clinical application.
What the study showed
The review describes how microbial metabolites (e.g., secondary bile acids via the bai operon, SCFAs, polyamines) participate in carcinogenic pathways through inflammation, immune evasion and metabolic reprogramming. No effect sizes (RR, OR, SMD) or confidence intervals are reported, as no meta-analysis or primary quantitative analysis was performed. The key empirical contribution cited is the demonstration that six enzymes encoded in the bacterial bai operon are necessary and sufficient to convert primary to secondary bile acids, a capacity absent from the human genome.
How it was done
Narrative review published in Frontiers in Cellular and Infection Microbiology (2026). No PROSPERO registration, systematic inclusion/exclusion criteria, or formal risk-of-bias assessment (AMSTAR-2 not applicable due to absence of quantitative synthesis). Covers analytical platforms (LC-MS, NMR) and mechanistic literature without defining a search time window or number of included studies.
Effect magnitude
No effect size quantified. The study is descriptive; no 95% CI is reported for any outcome.
Limitations
Narrative review without systematic methodology (no PRISMA; AMSTAR-2 not applicable): high risk of selection and confirmation bias. Does not distinguish causal evidence from association. Generalizes findings from preclinical models and small observational studies to the human context without quality weighting. Heterogeneity of populations, cancer types and analytical methodologies is not formally addressed.
In clinical practice
No change in clinical practice is supported by this study alone. Clinicians may use the text as a conceptual map of mechanistic pathways, not as a basis for prescription or screening. Microbial carcinogenesis biomarkers remain in a discovery phase, without prospective clinical validation.
What is still missing
Prospective longitudinal studies and RCTs testing interventions targeting the microbial metabolome in primary oncological outcomes are needed. Standardization of analytical platforms (LC-MS vs NMR) and cohorts is a prerequisite for replicability.