Aging and the Microbiome: precondition for gastrointestinal carcinogenesis
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Updated: Nov 4, 2026

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
Published on: July 28, 2010
Jonas Wizenty1, Michael Sigal2
1Department of Hepatology and Gastroenterology, Charité - Universitätsmedizin Berlin, Campus Virchow-Klinikum (CVK) and Campus Charité Mitte (CCM), Berlin, Germany; Berlin Institute of Health at Charité - Universitätsmedizin Berlin, BIH Biomedical Innovation Academy, BIH Charité Clinician Scientist Program, Berlin, Germany.
Abstract:
This review summarizes how aging-related changes in the gut microbiome contribute to gastrointestinal carcinogenesis. We highlight that cancer risk in aging is shaped not only by chronological age but largely by diet, lifestyle, environment, and their impact on microbial ecology. In healthy aging, microbial diversity is preserved with functional redundancy among short-chain fatty acid-producing commensals that support barrier integrity, immune regulation, and metabolic homeostasis. In unhealthy aging, loss of beneficial taxa, expansion of pathobionts, and accumulation of pro-inflammatory and genotoxic metabolites promote chronic inflammation, epithelial dysfunction, and DNA damage, thereby facilitating tumour development. Key microbial drivers include pks + Escherichia coli, enterotoxigenic Bacteroides fragilis, and Fusobacterium nucleatum, acting through genotoxic, inflammatory, and immune-evasive mechanisms. Although microbiome-targeted interventions such as diet modification, probiotics, faecal microbiota transfer, and phage-based strategies are promising, current evidence remains largely preclinical or observational. Overall, the gut microbiome is a central, modifiable mediator of aging-associated gastrointestinal cancer risk, but longitudinal studies are needed to establish causality and therapeutic efficacy.
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