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Cancer risk not linked to stem-cell division rates in organs

10 October 2016
Appeared in BioNews 872

Cancer risk is not linked to different rates of adult stem-cell division in organs, a study suggests.

The findings refute past research published last year which had suggested that different rates of adult stem-cell division, and therefore different rates of DNA error accumulation, might explain why certain organs in the body such as the bowel are at higher risk of cancer than others.

'We were surprised to find roughly the same mutation rate in stem cells from organs with different cancer incidence,' said Dr Ruben van Boxtel, lead researcher of the team. '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.'

Adult stem cells can be found in different organs of the body, where they replenish and repair tissue. In the study, which was published in Nature, scientists at UMC Utrecht in the Netherlands measured DNA errors in adult stem cells from the colon, small intestine, and the liver. Cells were taken from patients of a range of ages, from three to 87 years old.

They found that DNA error accumulation did not differ between stem cells, but remained stable at approximately 40 mutations a year.

However, the researchers found that different types of DNA errors arose between the organs. Dr van Boxtel suggests that the type of DNA error may explain why some organs have higher incidence of cancer.

The gradual build-up of DNA errors in adults stem cells is part of ageing, and is associated with various age-related diseases, including cancer. This is the first study to directly measure DNA errors in human stem cells from different organs and age groups.

Dr Lara Bennett, science communication manager at Worldwide Cancer Research, which funded the research, said: 'This new research by Dr van Boxtel and his group is important because it provides actual measured data on the rate of DNA error accumulation in human stem cells for the first time, and shows that perhaps not as much cancer risk is down to this type of "bad luck" process as has recently been suggested.'

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