Individuals who consume high amounts of red meat, which is rich in iron, may have an increased risk for developing bowel cancer, according to a study published in the journal Cell Reports.
Scientists at the Cancer Research UK, 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.
“We’ve made a huge step in understanding how bowel cancer develops. The APC gene is faulty in around eight out of 10 bowel cancers, but until now we haven’t known how this causes the disease," said Owen Sansom, deputy director of the Cancer Research UK Beatson Institute for Cancer Research. “It’s clear that iron is playing a critical role in controlling the development of bowel cancer in people with a faulty APC gene. And, intriguingly, our study shows that even very high levels of iron in the diet don’t cause cancer by itself, but rely on the APC gene."
The researchers said the results also suggest iron could be raising the risk of bowel cancer by increasing the number of cells in the bowel with APC faults. The more of these cells in the bowel, the greater the chance that one of these will become a starting point for cancer.
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 signaling 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 signaling remains inactive.
Scientists at the Cancer Research UK, 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.
“We’ve made a huge step in understanding how bowel cancer develops. The APC gene is faulty in around eight out of 10 bowel cancers, but until now we haven’t known how this causes the disease," said Owen Sansom, deputy director of the Cancer Research UK Beatson Institute for Cancer Research. “It’s clear that iron is playing a critical role in controlling the development of bowel cancer in people with a faulty APC gene. And, intriguingly, our study shows that even very high levels of iron in the diet don’t cause cancer by itself, but rely on the APC gene."
The researchers said the results also suggest iron could be raising the risk of bowel cancer by increasing the number of cells in the bowel with APC faults. The more of these cells in the bowel, the greater the chance that one of these will become a starting point for cancer.
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 signaling 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 signaling remains inactive.
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