The causal role of the gut microbiome in colorectal cancer

  • National Cancer Research Institute

  • curated by Dawn O'Shea
  • UK Medical News
Access to the full content of this site is available only to registered healthcare professionals. Access to the full content of this site is available only to registered healthcare professionals.

Research presented at the National Cancer Research Institution conference in Glasgow today (Monday, 4 November) suggests a causal relationship between gut microbiome and the development of colorectal cancer (CRC).

The research used Mendelian randomisation to examine the causal effect of the gut microbiome on CRC, combining data from genome-wide association studies (GWASs) of host genotype and gut microbiome variation from the Flemish Gut Flora Project and two German cohorts (n=3890) with the Genetics and Epidemiology of Colorectal Cancer Consortium (n=120,328).

The researchers found that the presence of an unclassified type of bacteria was associated with an increase in the risk of bowel cancer of up to 15 per cent.

Of 157 microbial traits (MTs) assessed in the GWAS of the gut microbiome, there was evidence for host genetic contributions to 13 MTs. Of these, there was evidence that the presence of a genus within a certain order of bacteria increased the risk of CRC by 8 per cent (95% CI, 2-15%; P=.02), with no strong evidence that the single-nucleotide polymorphism used as an instrument was associated with other traits, discounting the likelihood of pleiotropy.

The study confirms previous observational evidence suggesting that gut bacteria are more present in CRC cases than controls and provides further evidence that this may be due to a causal effect of these bacteria on CRC.

As the gut microbiome is a malleable trait, the discovery suggests a future role for diet manipulation on the risk of CRC.

Please confirm your acceptance

To gain full access to GPnotebook please confirm:

By submitting here you confirm that you have accepted Terms of Use and Privacy Policy of GPnotebook.