Mechanisms tumour promotion

Similarly, modulation of hepatocellular proliferation by peroxisome proliferators has been implicated in the mechanism of carcinogenesis. This can theoretically result in increased levels of mutation by increasing the frequency of replicative DNA synthesis as well as increasing the number of hepatocytes at risk. Furthermore, hepatocellular proliferation is probably involved in the promotion of growth of pre-neoplastic hepatocytes. There is clear evidence that di(2-ethylhexyl) phthalate causes acute and sustained hepatocellular proliferation under bioassay conditions which resulted in liver tumours in rats (Marsman et al., 1988). 

The symptomatic benefits of cannabis and its derivatives in patients with cancer has been discussed above, but considerable evidence has accumulated from in vitro and in vivo animal studies that cannabinoids may inhibit the growth of various types of tumour cell (For a review see Guzmdn s contribution in this volume and Guzman 2003). Possible mechanisms include the selective promotion of cancer cell apoptosis and inhibition of tumour vascularisation. Preliminary clinical studies have been initiated but no results reported at the time of writing. An issue to be determined is whether effects will be apparent at the tissue levels achievable in humans by systemic dosing—in some circumstances it may be preferable to seek ways to deliver the cannabinoid direct to the target site (Guzmdn 2003). 

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