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Biotech / Medical : T/FIF Portfolio -- Ignore unavailable to you. Want to Upgrade?

To: sim1 who wrote (1015)	7/3/1999 6:55:00 PM
From: Walkingshadow	Read Replies (1) \| Respond to of 1073

Stuart-- Thank you for the alert to the upcoming Nature Medicine article. Having not seen it, I could of course not comment. However, your post brings back a lurking doubt in my mind; I think I have posted on this before, but have not received any response. I wonder what you (or others) may think. In the release, it mentions anti-angiogenesis drugs being a promising method to treat cancer. This makes some amount of sense, in that cancer depends in part on neovascularization to grow and metastasize. Atherosclerosis also depends upon neovascularization (and thus, presumably, all the players associated with angiogenesis), because as a lesion gets bigger, it begins to outstrip its blood supply. My question relates to current trials to promote angiogenesis, and thereby treat entities such as peripheral vascular disease and ischemic cardiomyopathies. Although the attempt is made, in general, to deliver the agent (be it some form of VEGF or the gene) locally, still one wonders whether interventions which promote angiogenesis might, in the long run, also promote growth of tumors, perhaps even changing tumors which may have had a benign course into more aggressive neoplasms. Consider also that the target population for angiogenesis also exhibits a high prevalence of cancer relative to the general population, and so might be considered more "susceptible" to cancer in the first place; how might VEGF and other angiogenesis-promoting agents affect the likelihood that these people may demonstrate improvement in their PVD or CAD symptoms, yet may have increased risk of developing cancer? Might the "cure" ultimately be judged worse than the disease? Personally, I have lost a lot of my initial interest and enthusiasm for angiogenesis. Those I have spoken with working in the field are themselves rather skeptical that it will ever work out very well, except perhaps in a relatively small group of patients carefully selected. I would be curious to hear your thoughts on this matter. Although I said I can't say much about an article I haven't even read, I will say that, as stated in the report, MAPK is involved in a host of functions, and though I wouldn't want to dismiss it, I would be skeptical; the probability of unwanted and intolerable side effects associated with MAPK pathway inhibition would seem rather high. Another approach which I think is exceedingly clever involves the "Trojan Horse" strategy, whereby various things (notably, a modified Caspase-3) are taken up selectively by transformed cells, but result in their destruction; another strategy which I've become interested in involves the TRAIL (TNF-related apoptosis inducing ligand) pathway, which is being pursued by Lynch and company at IMNX. Both of these would seem to be less likely to be associated with unacceptable side effects, which of course, is one of the major drawbacks to most chemotherapeutic agents in existence today. As always, JMVHO; your thoughts most welcome. Walkingshadow