Omega-3 polyunsaturated fatty acids, in particular eicosapentaenoic acid, and docosahexaenoic acid have been shown to have multiple beneficial antitumour actions that affect the essential alterations that dictate malignant growth. In this review we explore the putative mechanisms of action of omega-3 polyunsaturated fatty acid in cancer protection in relation to self-sufficiency in growth signals, insensitivity to growth-inhibitory signals, apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion, and how these will hopefully translate from bench to bedside. 1. Introduction Fatty acids (FAs) are a diverse group of molecules. The fatty acyl structure represents the major building block of complex lipids and FAs should be regarded as one of the most fundamental categories of biological lipids [1]. Fatty acids are key nutrients that affect early growth and development, as well as chronic disease in later life. The benefits and potential risks of FAs go well beyond their defined role as fuel [2]. An FA containing more than one carbon double bond is termed polyunsaturated fatty acid (PUFA). The most important families in human metabolism are omega-6 (n-6) and omega-3 (n-3) PUFAs. Specific n-6 and n-3 PUFAs are essential nutrients, while the eicosanoids and docosanoids they derive have distinct biological activities affecting the prevalence and severity of cardiovascular disease, diabetes, inflammation, cancer, and age-related functional decline [1, 2]. Important n-3 PUFAs involved in human nutrition are α-linolenic acid (ALA or 18？:？3n-3), eicosapentaenoic acid (EPA or 20？:？5n-3), docosapentaenoic acid (n-3 DPA or 20？:？5n-3), and docosahexaenoic acid (DHA or 22？:？6n-3). ALA is the parent FA of the n-3 PUFA family. ALA is mainly found in the plant kingdom with high concentrations in flaxseed oil and perilla oil. It is also found in canola oil, soybean oil, and vegetable oils from where humans derive it in their diet. The human body is unable to readily synthesize ALA, which makes ALA, like linoleic acid (LA or 18？:？2n-6), the parent of the n-6 PUFA family, an essential fatty acid [1]. LA and ALA are converted to their respective n-6 and n-3 PUFA families by a series of independent reactions. However both pathways require the same enzymes for desaturation and elongation. This leads to competition between n-6 and n-3 PUFA for their metabolic conversion. The first step in the pathway requires Δ6 Desaturase [3, 4] which has a higher affinity for ALA than LA but due to the typically higher intake and concentration of LA there is
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