Is most cancer the result of “bad luck”?

Posted by The Evidence Blog on January 12, 2015

By Diane Allingham-Hawkins, PhD, FCCMG, FACMG, Senior Director, Genetic Test Evaluation Program and Technical Editing

Cancer is a major public health issue in the United States and around the world. It is estimated that approximately 1,665,540 new cases of cancer were diagnosed in the United States in 2014 and there were approximately 585,720 cancer deaths. Risk factors for cancer include lifestyle factors (e.g., smoking, alcohol use, obesity), environmental exposures (e.g., asbestos, formaldehyde), and heritable factors (e.g., variants in the BRCA1 or BRCA2 gene predisposing to breast, ovarian, and other cancers). A recent study, however, has suggested that the majority of cancers are due to “bad luck,” specifically, the accumulation of random genetic variants during cell division.

 

The authors of the study, which was published in the January 2, 2015, edition of the journal Science, studied the cell division rates for stem cells from 31 different tissue types and correlated their results with lifetime risk for cancers of those tissues. The authors found that the lifetime risk for cancer was highly correlated with the number of stem cell divisions for the tissue type. That is, the more stem cell divisions a tissue typically undergoes in a lifetime, the more common it is for tumors to grow in that tissue type. The authors then used complex statistical methods to classify the tissues into those with high versus low extra risk scores (ERS) based on the product of the lifetime tumor risk and the total number of stem cell divisions. Those with a high ERS (9 of 31 tissue types; referred to as D-tumors) had more influence from lifestyle, environmental, and heritable factors while those with a low ERS (22 of 31 tissue types; referred to as R-tumors) were more influenced by the number of cell divisions. The authors concluded that while D-tumors might be more amenable to primary prevention such as lifestyle changes as well as secondary prevention such as screening and early detection, the public health impact of R-tumors is only likely to be affected by secondary prevention.

So, does this study suggest that primary prevention of cancer should never be a public health goal? Of course not—after all, nearly 1 of 3 of the tumors studied were apparently impacted by lifestyle, environmental, and heritable factors. What the study does suggest, however, is that not all cancers can be prevented and, for these tumor types, effective secondary prevention methods should be the focus. Given that this is largely a modelling study dependent on statistical methods to draw conclusions, more research is needed to confirm the hypothesis put forth by the authors. It is sure to provide food for thought, however, for those public health policymakers concerned with cancer prevention.

Topics: Hayes Blog

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