Affiliations 

  • 1 Centre for Microbiome Medicine, Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore
  • 2 Centre for Microbiome Medicine, Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore; Department of Gastroenterology and Hepatology, Tan Tock Seng Hospital, National Healthcare Group, Singapore; State Key Laboratory of Digestive Disease, Department of Medicine and Therapeutics, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China; School of Pharmacy, Monash University Malaysia, Malaysia. Electronic address: sunny.wong@ntu.edu.sg
PMID: 42971668 DOI: 10.1016/j.bpg.2026.102155

Abstract

The gut microbiome can influence cancer susceptibility, progression, and treatment response. Microbes shape carcinogenesis through direct genotoxicity, epithelial barrier disruption, sustained inflammation, immune modulation, and the biotransformation of diet-derived substrates into bioactive metabolites. Diet is an important modifiable determinant of microbial community composition and function: Western dietary patterns may favour pro-carcinogenic microbial activities, whereas plant-rich, fibre-dense diets can support saccharolytic fermentation and commensal functions. These effects depend on substrate availability, microbial strain and host context. This review centres on colorectal and gastric cancers, with selected evidence from hepatocellular, pancreatic, breast and head-and-neck malignancies. Establishing causality remains central: most human evidence is associative, and mechanistic or interventional evidence is required for therapeutic or preventive translation. This review summarises the mechanistic roles of specific bacterial pathobionts, commensals and fungi across these cancer types, distinguishes observational, experimental and clinical interventional evidence for diet-microbiome interactions, and identifies translational priorities.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.