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Scientists discover how iron levels and a faulty gene cause bowel cancer

Thursday, August 09, 2012

Bowel Cancer UK statement in relation to 'Scientists discover how iron levels and a fauly gene cause bowel cancer.'

Deborah Alsina, CEO, Bowel Cancer UK said: "This is an exciting development and could be real breakthrough for helping to reduce the incidence of bowel cancer.  Whilst research needs to be carried out about how the amount of iron in a person's bowel can be reduced, it does appear to provide further evidence of just how important it is for people to have a balanced diet and to keep their intake of  red and processed meat down. We will follow treatment developments with interest and look forward to further trials as this could have a real bearing on the prevention of bowel cancer in the future."

Cancer Research UK press release


HIGH LEVELS of iron could raise the risk of bowel cancer by switching on a key pathway in people with faults in a critical anti-cancer gene, according to a study published in Cell Reports* today (Thursday).

Cancer Research UK scientists, based at the University of Birmingham and the Beatson Institute for Cancer Research in Glasgow, found bowel cancers were two to three times more likely to develop in mice with a faulty APC gene that were fed high amounts of iron compared to mice who still had a working APC gene.

In contrast, mice with a faulty APC gene fed a diet low in iron did not develop bowel cancer at all.

The study could also explain why foods such as red meat, which have high levels of iron, are linked to an increased risk of bowel cancer.

When the APC gene is deleted, two proteins are switched on that cause iron to build up in bowel cells. When this happens, a key cancer signalling pathway called wnt is switched on, causing cells to grow out of control.

In mice fed a diet with no iron, cells with a faulty APC gene were killed and bowel cancers did not develop.

Mice with a fully functioning APC gene did not develop bowel cancers, even when fed a diet high in iron. In these bowel cells, the iron accumulation proteins are turned off and wnt signalling remains inactive.