Gut bacteria could help fuel bowel cancer development

In collaboration with the Press Association

Bacteria can trigger inflammation in developing bowel tumours, which then drives the growth of the cancer, according to US research in mice.

In research published in Nature, the team show how bowel cancers lose a ‘defensive shield’ on their surface as they develop, which is found in healthy gut tissue.

This allows bacteria in the gut to penetrate the tumours, triggering inflammation and fuelling the tumour’s growth.

The work opens up the possibility of one day screening early-stage bowel tumours for specific molecules involved in inflammation to predict how aggressive they are likely to be.

The University of California scientists who carried out the research say it also suggests that drugs to target these molecules could be developed to help treat people with bowel cancer.

Professor Fran Balkwill from Cancer Research UK, who was not involved in the study, said: “This work provides an interesting explanation of why parts of the body’s normal ‘inflammatory response’ become faulty and drive the growth of bowel cancer. It suggests that common genetic faults in early-stage bowel tumours may cause the cancers to lose a protective barrier of cells.

“This allows gut bacteria to move into the tumour, which are then recognised by surrounding immune cells as invaders. The ensuing inflammatory reaction spurs the growth of the tumour.”

The link between inflammation and cancer was first discovered more than 100 years ago, and much is now known about how tumours hijack immune cells involved in inflammation to fuel their growth.

Several types of cancer are strongly linked to long-term (chronic) inflammation. For example, chronic hepatitis (inflammation of the liver) is linked to a higher chance of liver cancer, whereas inflammation caused by asbestos fibres is thought to drive mesothelioma.

But most cancers are not linked to such pre-existing conditions. Despite this, many tumours bear the hallmarks of inflammation, and seem to use immune cells to provoke and hijack the body’s normal inflammatory response.

The new study highlighted the role of two proteins involved in inflammation, known as interleukin-17 (IL-17) and interleukin-23 (IL-23).

Professor Balkwill said that it was fascinating research that “adds another dimension the traditional view of tumours ‘actively recruiting’ immune system cells”.

But, she said, “only time will tell if this definitely happens in people with cancer”.

“A possible next step is to test tissue samples from early-stage bowel cancers for the inflammatory molecules identified in this study, IL-17 and IL-23, and see if higher levels are associated with worse survival. This could be relatively simple, given that several countries have tissue samples from bowel screening programmes,” she added.

References

  • Grivennikov, S.I., Wang, K., Mucida, D., Stewart, C.A., Schnabl, B., Jauch, D., Taniguchi, K., Yu, G.Y., Österreicher, C.H., Hung, K.E. & (2012). Adenoma-linked barrier defects and microbial products drive IL-23/IL-17-mediated tumour growth, Nature, DOI: 10.1038/nature11465