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To: Walkingshadow who wrote (1030)7/9/1999 4:18:00 AM
From: sim1  Read Replies (1) | Respond to of 1073
 
Regretably, I don't have the necessary background to make an intelligent comment here. Like many others here at SI, I get great value from the many thoughtful posts and quality analysis by people who understand both the business and science of this industry. For now, I simply try to help "carry water" for others (hopefully not spilling too much along the way), and try to provide relevant information that I might occasionally run across. It is my hope to increase my contributions as I learn.

Regarding you're thoughts on angiogenisis, I can only respond (and agree) from a personal perspective. If it were my bare buns perched on some cold physicians examination table and I was given an option of an angiogenisis drug that might possibly help my particular problem but, the drug could also trigger some sort of biological catastrophe in other parts of my body, the answer would be clear - thanks, but no thanks. I'll take my chances without their "miracle drug". It seems to me that the only way for any angiogenisis drug to work safely and effectively would be for it to work in conjunction with some technology that has the ability to target and restrict the angiogenisis to some designated area in the body.

Below is the abstract from the referenced Nature article. I'm not (yet) a subscriber and therefore don't have access to the full article. I hope this is helpful.

Thanks for your response.



July 1999 Volume 5 Number 7 pp 810 - 816


Blockade of the MAP kinase pathway suppresses growth of colon tumors in vivo

Judith S. Sebolt-Leopold1, David T. Dudley1,
Roman Herrera1, Keri Van Becelaere1, Amy
Wiland1, Richard C. Gowan1, Haile Tecle2,
Stephen D. Barrett2, Alexander Bridges2, Sally
Przybranowski3, W.R. Leopold3 & Alan R. Saltiel1


The mitogen-activated protein kinase pathway is thought to be essential in cellular growth and differentiation. Here we report the discovery of a highly potent and selective inhibitor of the upstream kinase MEK that is orally active. Tumor growth was inhibited as much as 80% in mice with colon carcinomas of both mouse and human origin after treatment with this inhibitor. Efficacy was achieved with a wide range of doses with no signs of toxicity, and correlated with a reduction in the levels of activated mitogen-activated protein kinase in excised tumors. These data indicate that MEK inhibitors represent a promising, noncytotoxic approach to the clinical management of colon cancer.


1. Department of Cell Biology, Parke-Davis Pharmaceutical Research, Division of Warner-Lambert, 2800 Plymouth Road, Ann Arbor, Michigan 48105, USA
2. Department of Chemistry, Parke-Davis Pharmaceutical Research, Division of Warner-Lambert, 2800 Plymouth Road, Ann Arbor, Michigan 48105, USA
3. Department of Cancer Research, Parke-Davis Pharmaceutical Research, Division of Warner-Lambert, 2800 Plymouth Road, Ann Arbor, Michigan 48105, USA

Correspondence should be addressed to J S Sebolt-Leopold.