Scientists at the University of Liverpool have identified a type of E. coli bacteria that may encourage the development of colon cancer.
The Liverpool team had previously shown that people with colon cancer and with the inflammatory bowel diseases, Crohn's disease and ulcerative colitis, have high numbers of a sticky type of E. coli in their colons.
The team have now found that E. coli bacteria, which carry pks genes that encode a toxin that damages DNA in the cells of the gut lining, are more commonly found in the colons of patients that have inflammatory bowel disease and colon cancer than those that do not have these conditions. Approximately two thirds of patients with colon cancer carry these E. coli compared with one in five with a healthy colon.
Research, in collaboration with the University of North Carolina, showed that mice with colitis are more likely to carry these E. coli and they often develop colon cancer when carrying E. coli containing pks genes. They did not, however, develop cancer with identical E. coli that did not contain pks. They also found that the presence of E. coli carrying the pks genes did not appear to increase inflammation of the gut.
Professor Jonathan Rhodes, from the University's Institute of Translational Medicine, said: "The fact that the pks-positive E. coli seemed to promote colon cancer in mice without causing increased inflammation led us to investigate its possible role in human colon cancer. The marked increase in the presence of these bacteria in the colon, not only in patients with inflammatory bowel disease, but also in patients with colon cancer who do not have inflammatory bowel disease, suggests that damage caused to DNA, as a result of the toxin that the pks genes produce, may promote the development of colon cancer."
Dr Barry Campbell, co-author of the research at the University of Liverpool, said: "The research suggests that E. Coli has a much wider involvement in the development of colon cancer than previously thought. It is important to build on these findings to understand why this type of bacteria, containing the pks genes, is present in some people and not others."
The Liverpool team involved in this study were also the researchers that discovered that dietary agents, particularly plantain and broccoli, could prevent the uptake and transport of E. coli through cells in the gut. They also found that fat emulsifiers in processed food encouraged the movement of bacteria through the cells.
The research, supported by North West Cancer Research Fund, Crohn's & Colitis UK, and the National Institute for Health Research, is published in the journal Science.
Notes to editors:
1. The University of Liverpool is one of the UK's leading research institutions with an annual turnover of £410 million, including £150 million for research. Liverpool is ranked in the top 1% of higher education institutions worldwide and is a member of the Russell Group. Visit www.liv.ac.uk
2. The National Institute for Health Research (NIHR) is funded by the Department of Health to improve the health and wealth of the nation through research. Since its establishment in April 2006, the NIHR has transformed research in the NHS. It has increased the volume of applied health research for the benefit of patients and the public, driven faster translation of basic science discoveries into tangible benefits for patients and the economy, and developed and supported the people who conduct and contribute to applied health research. The NIHR plays a key role in the Government's strategy for economic growth, attracting investment by the life-sciences industries through its world-class infrastructure for health research. Together, the NIHR people, programmes, centres of excellence and systems represent the most integrated health research system in the world. For further information, visit the NIHR website.
This news release describes independent research funded by the National Institute for Health Research (NIHR). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health.
Journal
Science