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New research suggests cancer isn’t just ‘bad luck’ after all (unsurprisingly)

New research funded by Worldwide Cancer Research provides a major piece of the puzzle for scientists trying to figure out just how much of our cancer risk is unavoidable.

Worldwide Cancer Research scientist Dr Ruben van Boxtel and his team at UMC Utrecht in the Netherlands have gathered evidence directly from human stem cells which suggests that although accidental ‘bad luck’ may play a part in some cancers, it is perhaps not as much as previously suggested.

The work, published in Nature today, is particularly important because it is the first time that scientists have directly measured DNA mutations in adult human stem cells from different organs, and at different ages.

What's the research all about?

From cigarette smoke to sunshine, our cells are constantly bombarded by DNA damaging forces which, given enough time, can sometimes lead to cancer. We can do something to protect our DNA against these external attacks. But sometimes there is no outside force. Sometimes it’s our own cells which make mistakes– cell division and other unseen processes accidentally introduce ‘random mutations’ that go unrepaired.

Controversial research published last year by a US group suggested that differences in the rate of accumulation of these types of unavoidable 'bad luck' DNA mutations gained through normal cell division might heavily influence our risk for some cancers over others. But this research, and the subsequent research published by another US group which disputed this claim is based on computer modelling, in other words, no one had yet actually measured and compared the levels of DNA mutations in human stem cells- the 'seed cells' of all organs in our body.

So Dr van Boxtel and his team set out to do this. Their aim was to measure just how many of these accidental, and unavoidable DNA mistakes accumulate over the course of our lives. They studied adult stem cells isolated from left over tissue samples taken as part of routine patient biopsies, focusing on cells from the colon (large bowel), liver, and small intestine as these organs have starkly different rates of cancer. As many as 110 new cases of bowel cancer are diagnosed every day in the UK, compared to just 15 cases of liver cancer. Cases of cancer in the small intestine are even rarer.

The researchers also looked at stem cells from a range of different ages- from patients 3 years old all the way up to 87 years. By measuring the different numbers of DNA mutations in this wide variety of samples they hoped to gather a good idea of just how the accumulation of random, unavoidable DNA mutations over time might be linked to age and cancer risk.

What did the research find?

The researchers' findings were unexpected. Instead of the mutation rate being higher in tissues more prone to cancer, the results instead showed that random DNA mutations actually gather at a rather sedate rate of about 40 mutations a year, regardless of the type of organ the stem cell comes from, or age of the patient.

“We were surprised to find roughly the same mutation rate in stem cells from organs with different cancer incidence,” says Dr van Boxtel. “This suggests that simply the gradual accumulation of more and more ‘bad luck’ DNA errors over time cannot explain the difference we see in cancer incidence– at least for some cancers.”

This part of the finding goes some way against the original claim that the individual risk for developing cancer in different organs is mainly influenced by numerical differences in unavoidable mutations caused by differences in stem cell turnover rate.

But there’s more. Although the team didn’t find any real differences in overall numbers of accidental DNA mutations in stem cells, they did notice a difference in the type of unavoidable DNA mutations between the tissues, which Dr van Boxtel says could ultimately turn out to partly explain increased rates of cancer in some organs like the bowel.

“It seems ‘bad luck’ is definitely part of the story,” says Dr van Boxtel. “But we need much more evidence to find out how, and to what extent. This is what we want to focus on next.”

What does this mean for you?

Right now, not much. Unless like me you get excited watching real science unfold before your very eyes.

We already know that for some cancers lifestyle factors like smoking and diet are very important in terms of moderating your cancer risk, as we’ve outlined in earlier blogs about obesity, and processed meat. And it's a sad reality that for many with cancer, frustratingly, nothing could be done to prevent it.

But the real impact of this work is in the new evidence, the new knowledge it gives to researchers trying to find out how to prevent and treat cancer. There is still so much we need to know about how cancer starts. The more we can find out about this, the closer we get to developing new treatments, and finding new ways to tackle it.

So this research is very exciting in terms of helping to settle some rather ‘vigorous scientific debate’ which at times has got pretty heated. But it’s much more than that. The real importance of this work, the bit that really matters, shines through when viewed from the long-range angle- where beating cancer is the goal.

How did Worldwide Cancer Research specifically help this research?

Worldwide Cancer Research was a major funder on this project, which only started at the beginning of this year and has already yielded such important findings. You can read more about Dr van Boxtel's project with us here.

“The support from Worldwide Cancer Research made a huge difference to this project,” says Dr van Boxtel. “With this funding we were able to expand our aims. We could add more tissue samples from other organs, which was crucial to really make a link with cancer in a meaningful way, and begin to understand how these processes are involved in cancer.”

“I am immensely grateful to your supporters for helping to make this research possible.”

 

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