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These effects appear to be mediated, in linseed oil part, linseed oil by the interaction of AA-derived eicosanoids with growth factors and oncogenes, (24,25,27,28,30,31) and their effects on protein kinases. (26,31) Administration of long-chain n-3 PUFAs (EPA and DHA) is associated with suppression of these processes via modulation of eicosanoid synthesis. In vitro studies, using low linseed oil FFA concentrations and experimental conditions nonconducive to lipid peroxidation, support the contention that cancer cell growth is enhanced by AA-derived eicosanoids and that their effects are counteracted by long-chain n-3 PUFAs. (19,32,33) It has also been shown that tumor cells produce a potent mitogenic compound from LA (13-hydroxyoctadecadienoic acid) via a lipoxygenase pathway, and that n-3 PUFAs inhibit cellular uptake of LA, thereby reducing the rate of cell proliferation. (34) Additionally, incorporation of EPA, DHA, and GLA into cancer cell membranes may alter cancer growth and metastasis by mechanisms independent of their effects on eicosanoid synthesis.
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