Stem Cell Study finds Cancer Not Mainly Down To ‘Bad Luck
A controversial study published in 2015 suggested that the majority cases of cancer are simply down to “bad luck” – that random DNA mutations in adult stem cells that are just that, random, and not caused by lifestyle factors. A new study, however, contradicts this claim; bad luck may play a role cancer development, but research has found that it is unlikely to be the primary contributor.
Cancer occurs as a result of DNA mutations that change the way that cells grow and divide. These mutations can result in cells becoming out of control; they grow and divide inordinately, gathering faults along the way that make them become cancerous.
Some DNA mutations can be inherited from our parents; others can be acquired during our lifetime through lifestyle factors, such as smoking and sun exposure.
It is well established, however, that some organs are more susceptible to cancer than others, and these variations cannot possibly all be accounted for by lifestyle factors.
A study published in the journal Science in January 2015, suggested that 22 out of 31 cancer types – including ovarian, pancreatic, and bone cancers – occur as a result of random “accidental” mutations that occur in normal adult stem cells as they divide.
New research, however – led by Dr. Ruben van Boxtel of the Department of Genetics at University Medical Center Utrecht in the Netherlands – suggests these “bad luck” mutations do not contribute to cancer development as much as last year’s report claims.
The results – published in the journal Nature – come from the first ever study to assess the accumulation of DNA mutations in human adult stem cells isolated from various organs at different life stages.
Dr. van Boxtel and colleagues assessed the rates and patterns of DNA mutations in normal adult stem cells taken from the colon, small intestine, and liver of human donors aged 3-87 years.
The researchers found that regardless of the age of the patient or the organ the stem cells derived from, the number of DNA mutations that accumulated in the stem cells over time remained stable, at an average of 40 a year.
“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,” Boxtel added.
The team identified differences in the types of random DNA mutations between stem cells from different organs, which might partially explain why some organs are more prone to cancer than others.
“So 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.”
Dr. Lara Bennett, science communication manager at Worldwide Cancer Research – which funded the study – believes the team’s findings help shed light on why some types of cancer are more common.
“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.”