We know of at least eight viruses which cause cancer in humans, but apart from Helicobacter pylori there are no firmly established cases of bacteria causing tumours. Having said that, there are a number of bacteria which have been shown to be associated with certain cancers, but the relationship between cancer and bacteria is not as clear cut as in the casue of human tumour viruses. A recent paper in PLOS ONE adds to the list of bacteria associated with particular tumours.
The human intestinal microbiota inhabits a complex and diverse environment populated by hundreds of different bacterial species. These bacteria are regulated in the gut by the mucosal immune system, which is made up of a complex network of functions and immune responses aimed at maintaining a cooperative system between the intestinal microbiota and the host. In a healthy gut these bacteria maintain homeostasis with the host. However, when an imbalance, or bacterial dysbiosis, occurs in the gut, the host may experience inflammation and a loss of barrier function. Bacterial dysbioses have been linked to several diseases including ulcerative colitis, Crohn’s disease and colorectal cancer (CRC).
No single bacterial species has been identified as a risk factor for CRC, but recent studies report an increase in the abundance of Fusobacterium in human colorectal tumors compared to controls. These studies suggest that Fusobacterium may be associated with the later stages of CRC, but it is unknown if they play a role in the early stages of colorectal carcinogenesis. While the causes of colorectal cancer are not fully known, it is becoming increasingly clear that the gut microbiota provide an important contribution.
Fusobacterium Is Associated with Colorectal Adenomas. (2013) PLoS ONE 8(1): e53653. doi:10.1371/journal.pone.0053653
The human gut microbiota is increasingly recognized as a player in colorectal cancer (CRC). While particular imbalances in the gut microbiota have been linked to colorectal adenomas and cancer, no specific bacterium has been identified as a risk factor. Recent studies have reported a high abundance of Fusobacterium in CRC subjects compared to normal subjects, but this observation has not been reported for adenomas, CRC precursors. We assessed the abundance of Fusobacterium species in the normal rectal mucosa of subjects with (n = 48) and without adenomas (n = 67). We also confirmed previous reports on Fusobacterium and CRC in 10 CRC tumor tissues and 9 matching normal tissues by pyrosequencing. We extracted DNA from rectal mucosal biopsies and measured bacterial levels by quantitative PCR of the 16S ribosomal RNA gene. Local cytokine gene expression was also determined in mucosal biopsies from adenoma cases and controls by quantitative PCR. The mean log abundance of Fusobacterium or cytokine gene expression between cases and controls was compared by t-test. Logistic regression was used to compare tertiles of Fusobacterium abundance. Adenoma subjects had a significantly higher abundance of Fusobacterium species compared to controls (p = 0.01). Compared to the lowest tertile, subjects with high abundance of Fusobacterium were significantly more likely to have adenomas (OR 3.66, 95% CI 1.37–9.74, p-trend 0.005). Cases but not controls had a significant positive correlation between local cytokine gene expression and Fusobacterium abundance. Among cases, the correlation for local TNF-α and Fusobacterium was r = 0.33, p = 0.06 while it was 0.44, p = 0.01 for Fusobacterium and IL-10. These results support a link between the abundance of Fusobacterium in colonic mucosa and adenomas and suggest a possible role for mucosal inflammation in this process.