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Biotech / Medical : AMEV-Applied Molecular Evolution -- Ignore unavailable to you. Want to Upgrade?

To: tuck who wrote (25)	12/31/2001 3:18:02 PM
From: scaram(o)uche	Respond to of 164

Yeah, well, it's wait and see. If there is to be a day where indirect attacks on a tumor will contribute to "cancer as a chronic disease", animal studies (and now the phase I that you cited) indicate that anti-integrin therapy is a contending player. My personal feel -- at this time -- is that the complexity of effective cocktails will make it difficult to commercialize any given component. FDA has to act in an enlightened fashion. I agree with Peter...... President Bush, get us an FDA Commissioner!! This has grown to be absurd.

To: tuck who wrote (25)	1/1/2002 11:27:10 AM
From: scaram(o)uche	Respond to of 164

Ah, got it! Well, sorta got it. The individual who did the soundbit probably got the lead from BioCentury. There's a paper in the latest issue of Nature Medicine..... January 2002 Volume 8 Number 1 pp 27 - 34 Enhanced pathological angiogenesis in mice lacking 3 integrin or 3 and 5 integrins Louise E. Reynolds1, 4, Lorenza Wyder1, 4, Julie C. Lively2, Daniela Taverna2, Stephen D. Robinson1, Xiaozhu Huang3, Dean Sheppard3, Richard O. Hynes2 & Kairbaan M. Hodivala-Dilke1 Inhibition of v3 or v5 integrin function has been reported to suppress neovascularization and tumor growth, suggesting that these integrins are critical modulators of angiogenesis. Here we report that mice lacking 3 integrins or both 3 and 5 integrins not only support tumorigenesis, but have enhanced tumor growth as well. Moreover, the tumors in these integrin-deficient mice display enhanced angiogenesis, strongly suggesting that neither 3 nor 5 integrins are essential for neovascularization. We also observed that angiogenic responses to hypoxia and vascular endothelial growth factor (VEGF) are augmented significantly in the absence of 3 integrins. We found no evidence that the expression or functions of other integrins were altered as a consequence of the 3 deficiency, but we did observe elevated levels of VEGF receptor-2 (also called Flk-1) in 3-null endothelial cells. These data indicate that v3 and v5 integrins are not essential for vascular development or pathological angiogenesis and highlight the need for further evaluation of the mechanisms of action of v-integrin antagonists in anti-angiogenic therapeutics. 1. Cell Adhesion and Disease Laboratory, Richard Dimbleby Department, Imperial Cancer Research Fund, St. Thomas' Hospital, London, UK 2. Howard Hughes Medical Institute, Center for Cancer Research, MIT, Cambridge, Massachusetts 02139 USA 3. Lung Biology Center, University of California, San Francisco, California, USA 4. L.E.R. and L.W. contributed equally to this study.