I am also very interested in this question! There are evidences that dietary n-3 PUFA inhibit progression of carcinogenesis by suppression of arachidonic acid – derived eicosanoid biosynthesis. Eicosanoids generated from AA, such as PGE2, leukotriene B4, thromboxane A2 and others were positively linked to carcinogenesis in their promotion of tumor cell survival and, additionally, they were found at higher concentrations in cancer cells than in normal cells. Also interesting is that the formation of AA-derived eicosanoids is decreased not only by n-3 PUFAs but also by eicosanoids derived from them, and some of these eicosanoids have an even more inhibitory effect. So, the ways to inhibit the generation of eicosanoids might be beneficial for treatment since they seem to interefere on many levels with the carcinogenic progression - production of ROS, inhibition of apoptosis, modulation of inflammation processes, proliferation, angiogenesis, etc..
up regulation of COX 2 has been evaluated in various cancers - colon, pancrease, head and neck etc
molecular mechanism is attributed to
cells overexpressing cox 2 undergo phenotypic changes that could enhance tumorigenic potential- increased proliferative potential through PGE2 mediated release of epidermal growth factors and actions through cytokines in autocrine and paracrine fashion
tumor progression due to ability to induce angiogenesis- VEGF
Evation of apoptosis - bcl 2 alteration
tissue invasion and metastasis - increased MMP ETC
Thus arachidonic acid pathway is described in every hallmark of cancer