Abstract
Linoleic acid, an n-6 polyunsaturated fatty acid, is essential for normal mammary tissue development, at least in part because it provides the metabolic precursor required for the biosynthesis of key eicosanoids. A similar requirement applies to the growth of estrogen-independent but apparently not to estrogen-dependent rodent mammary and human breast carcinoma cells in vitro. By way of lipoxygenase products, n-6 fatty acids also regulate expression of the invasive phenotype. High-fat, linoleic acid-rich diets promote chemically induced rat mammary carcinogenesis, virally induced mouse mammary tumor development, and the growth and metastasis of estrogen-independent human breast cancer cells in athymic nude mice. In contrast, saturated fatty acids have no discernible effects on mammary carcinogenesis or progression. Most mechanistic studies have focused on the cyclooxygenase and lipoxygenase products of n-6 fatty acid metabolism, and support is accumulating for interactions between these eicosanoids and growth factors and oncogenes. The investigation of dietary fatty acids in prostate cancer is at an early stage and has been handicapped by a lack of satisfactory animal models. However, there are indications that the n-6 fatty acids perform functions in experimental prostate cancer progression similar to those described for breast cancer.
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