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The Preventability of Cancer: Stacking the Deck.

Over the past year, major attention has focused on whether cancer arises by chance or as a result of external factors that, if modifiable, could imply that cancer is preventable and not simply the result of random events. The underlying truth of this debate has major implications for everything from the Vice President’s Moonshot1—are we preventing cancer or only aiming to treat it after it develops?—all the way to policies and practices that may determine cancer risk for future generations. Although Vogelstein and colleagues2 have previously advocated for prevention as the first line of attack in the war on cancer—holding treatment in reserve, as plan B, when prevention fails—members of that same research group have also recently contended that cancer is largely due to chance, a position that has received far more attention.3 The basis for this later assertion is the underlying relation of increasing cancer risk with age,4 or, as modeled recently by Tomasetti and Vogelstein,3 the underlying relation of increasing cancer risk with number of stem cell divisions. This increasing risk with age or stem cell division can be explained in at least 2 non–mutually exclusive ways, the relative contributions of which are currently under intense debate. Tomasetti and Vogelstein, on the one hand, propose that random, accumulated mutations during cell division are largely responsible for this relation—essentially that “bad luck” drives the development of most cancers.3 Wu and colleagues,5 on the other hand, as well as several other investigators, posit an alternative hypothesis whereby external—or extrinsic or exogenous—factors that increase the rate of cell turnover or the chance of genomic damage during cell division are greater drivers of cancer risk. In classic epidemiology, we might refer to these external factors as environmental or lifestyle factors. Examples of environmental influences on cancer risk are abundant. If we go back in history, one of the first examples is the high incidence of scrotal cancer among young chimney sweeps in 16thand 17th-century Britain, which declined with the banning of “chimney boys.”6 This epidemic of scrotal cancer was not due to chance but rather to exposure to a carcinogen, coal tar. Likewise, classic studies of migrants that compared individuals who migrated with those who remained in their home countries clearly show that cancer risk is responsive to the external environment of the adopted country, be it sunlight or diet or other external factors.7 Finally, the dramatic increase in lung cancer mortality with the popularity of cigarette smoking in the 1900s and its subsequent decline by one-third over the past 25 years also speak to the strong influence of environmental factors on cancer risk.