Cancer risk: Prevention is crucial

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Science  13 Feb 2015:
Vol. 347, Issue 6223, pp. 728
DOI: 10.1126/science.aaa6462

As cancer prevention scientists, we read C. Tomasetti and B. Vogelstein's Report “Variation in cancer risk among tissues can be explained by the number of stem cell divisions” (2 January, p. 78) with considerable interest. Many of the findings support previous research: Cancers vary in preventability, and the cancers that cause the most mortality in developed countries (lung and colon) are highly preventable (1). However, other findings in the Report do not reflect the current evidence.

For example, many of the “R-tumor” type cancers that the authors hypothesize to be unlikely to be preventable have well-known modifiable risk factors, such as tobacco and alcohol use for esophageal and head and neck cancers, radon exposure for lung cancer in nonsmokers, and ultraviolet light exposure for melanoma (1). There is also well-documented variation in cancer incidence rates for these and other cancers, globally and due to migration, as well as over time (1). These kinds of changes do not seem to be compatible with the theory that these cancers originate primarily from random stem cell mutations.

Tomasetti and Vogelstein found an interesting statistical relationship between rates of stem cell division and cancer rates in selected tissues, but they overinterpret the results by implying a causal relation. Emerging evidence suggests that stem cell division rates, and errors in division, are not simply a product of time and chance; they vary due to many external influences, including obesity, environmental pollution, infections, and inflammation (2, 3).


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