The preventability of cancer: Stacking the deck
A partir des données des cohortes américaines "Nurses’ Health Study" et "Health Professionals Follow-up Study" incluant respectivement 89 571 femmes et 46 339 hommes, cette étude prospective évalue le nombre de cancers et de décès par cancer évitables grâce à la modification des modes de vie et des comportements de santé
Résumé en anglais
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.