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Dietary omega-3 fatty acids, genetic variation and risk of breast and prostate cancers.

Breast (BrC) and prostate cancers (PCa) are the two most common tumors in women and men, respectively, in Western countries [1, 2]. Both tumors are hormonedependent cancers in their early stages. They share some similar risk factors like age, obesity, and genetic factors such as family history, ethnicity or genetic variants [3, 4]. Nevertheless, the mechanisms of carcinogenesis of these complex, multifactorial diseases are still incompletely understood because the known risk factors explain only a small fraction of the new cancers diagnosed. Other potential causal mechanisms were thus explored. There are large regional distinctions in cancer incidence of both breast and prostate cancers [1]. Women moving from countries like Japan with a formerly low breast cancer risk, for example, to the United States, where breast cancer is common, developed the same risk within a few decades [5, 6]. Prostate cancer incidence also varies markedly throughout different countries. Migrant Japanese and Chinese men in the USA have a higher incidence and mortality from prostate cancer than do their relatives in Japan and China [7, 8]. Thus, the environment clearly modulates the risk of developing these cancers. Diet has been identified as a possible factor but studies pursued in the last years produced conflicting results [9– 11]. It is postulated that dietary components might influence early carcinogenesis or tumor progression by exerting inflammatory or antiinflammatory effects, and some are thought to bear protective abilities, like vitamins D and E, selenium, lycopene, or unsaturated fatty acids, notably polyunsaturated omega3 fatty acids (ω– 3 PUFA) of marine origin [12]. Due to the inconsistent findings of the effect of polyunsaturated fatty acids on BrC and PCa incidence, the question arose if humans would exhibit a differing susceptibility to these essential nutrients, perhaps on account of genetic variation that would predispose its carrier for a variation in cancer risk. Several studies have been published in the last years examining these interactions, which shall be reviewed in this article, emphasizing recent epidemiological and gene/diet interaction findings.