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A diagram of the bowelsJust a quick one. We’ve written before about the links between inflammation and cancer, and couched a lot of what we’ve written in all sorts of caveats like ‘may’ and ‘might’.

Well, last week, a few more of those caveats fell away, and the picture became just a little bit clearer.

Scientists in the US have, for the first time, demonstrated that chronic inflammation leads to pre-cancerous problems, DNA damage and, ultimately, bowel and stomach cancer, amongst mice who have been bred to have sluggish ‘DNA repair mechanisms’.

This is a really important finding.

All of our cells contain proteins whose job it is to scan our DNA for problems and repair them – this forms a key part of our natural defence against cancer. And because of natural genetic variation, different people can have slightly different versions of these proteins.

For example, my versions of these proteins may work slower (or faster) than yours, or make more (or fewer) mistakes.

The study showed that mice bred to have ‘slow’ versions of these proteins AND who have low-level (chronic) inflammation (caused – in this study – by inducing an ‘irritable bowel syndrome’-like condition, or by the bacterium H. pylori), had higher rates of cancer than ‘normal’ mice who had the same inflammation.

This helps to explain why some people are more at risk of bowel cancer than others. According to this theory, inflammation causes gut cells to divide faster; mistakes accrue; but people born with lethargic DNA repair machinery fail to repair the damage in time, so are more likely to get cancer.

It’s an absolutely classic case of the sort of gene-environment interaction Ed’s been writing about recently.

And, even though it’s only research on mice, not people, it gives the research community confidence that it’s on the right track, and that inflammation is one of the cutting-edge fields in cancer research at the moment.

Henry

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