This month’s Science Magazine features a paper by two Johns Hopkins scientists that provides support for a more refined theory of causation in a number of types of cancer.  The article by Drs. Christian Tomasetti and Bert Vogelstein entitled “Variation in Cancer Risk Among Tissues Can Be Explained By The Number of Stem Cell Divisions” includes the following abstract:

Some tissue types give rise to human cancers millions of times more often than other tissue types. Although this has been recognized for more than a century, it has never been explained. Here, we show that the lifetime risk of cancers of many different types is strongly correlated (0.81) with the total number of divisions of the normal self-renewing cells maintaining that tissue’s homeostasis. These results suggest that only a third of the variation in cancer risk among tissues is attributable to environmental factors or inherited predispositions. The majority is due to “bad luck,” that is, random mutations arising during DNA replication in normal, noncancerous stem cells. This is important not only for understanding the disease but also for designing strategies to limit the mortality it causes.

This finding may have broad implications in determining what may cause the cancer at issue in a particular case.  This article concludes that the incidence or lifetime risk of many cancers directly correlates to the number of stem cell divisions in the tissue involved in the cancer.  This correlation appears to be, in many cases, independent of any environmental or external factors.  Because the article provides a potential explanation for the cause of many types of cancer, this may allow experts to use rate of stem cell division as a causation argument in lieu of saying the cause is “idiopathic.”

Interestingly, among the cancers that have a higher rate of stem cell divisions are acute myelogenous leukemia and chronic lymphocytic leukemia, two types of cancer that are prevalent in matters involving allegations of exposure to trace benzene. This fact will certainly be the source of future argument regarding general causation.  We expect there to be future scientific inquiry into the findings in this article, but the findings alone do raise important issues.  Further studies in this area may provide further support for arguing against an environmental correlation between cancer risk and exposure in cases where the cancer involved has a high rate of stem cell division.  We expect that this study and future studies will have a significant effect in matters involving allegations of toxic exposure.