Gut Microbiome May Predict Progression of Colon Cancer
The gut microbiome has been linked to a wide range of health indicators over recent years and, according to a recent study published in Genome Medicine, may help predict prognosis of patients with colon cancer. In this study, the microenvironment of colon cancer tumors had an abundance of Fusobacterium and Providencia species, perhaps identifying a microbiome signature that predicts patient prognosis.
The link between alterations in the gut microbiome and colon cancer have been shown in previous studies, with tumor tissue showing greater bacterial diversity and abundance of pathogenic bacteria than the surrounding healthy tissue. Although previous researchers have identified several pathogenic bacteria associated with colon cancer, they have not defined a single microbiome signature associated with development and progression of colon cancer.
Lead author Michael Burns and his colleagues at the University of Minnesota sequenced the microbiome of 44 primary tumor and 44 patient-matched normal colon tissues. Similar to previous researchers, Burns and his colleagues found increased microbial diversity, in particular an increase in Fusobacterium and Providencia species. The increase in these species presumably contributed to a significant enrichment of virulence-associated bacterial genes in the tumor microenvironment, suggesting that the alterations in the microbiome contributes to development and progression of colon cancer.
Although previous research has shown Fusobacterium to cause cancer, this was the first study to show an association between Providencia and colon cancer. According to the researchers, the results provide a starting point for future investigations to predict prognosis and response to treatment, although further research will be required to establish a causal link between the microbiome signature and colon cancer.
Source: Burns MB, et al 2015. Virulence genes are a signature of the microbiome in the colorectal tumor environment. Genome Medicine;7(1).