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TSRI Scientists Discover Naturally-Occurring Mechanism Involved In Regulation Of Angiogenesis; New Anti-Cancer Therapeutic Agents Are Suggested

La Jolla, CA - February 6, 1998 -- For years scientists have studied angiogenesis, the process whereby new blood vessels are formed from pre-existing ones. Except in a few special circumstances, it does not occur in the normal adult. However, angiogenesis plays a key role in a number of diseases associated with new blood vessel growth such as cancer, diabetic retinopathy, macular degeneration and arthritis. Many scientists have worked to develop methods to promote the selective obliteration of new blood vessel cells that could ultimately lead to regression of the neovascularization associated with these diseases. Now, scientists at The Scripps Research Institute have not only uncovered a mechanism to help explain angiogenesis activity, but have developed a recombinant form of a protein fragment that blocks angiogenesis and tumor growth in an in vivo experimental model. This may provide a potentially novel therapeutic approach for diseases associated with neovascularization.

"Our findings show how an enzyme that promotes angiogenesis can be naturally cleaved to produce a fragment that inhibits this process. We determined that this enzyme fragment likely plays a role in normal blood vessel development. Thus, by taking advantage of this knowledge we have incorporated this into an anti-angiogenesis strategy to block tumor growth," according to one of the paper's authors, David A. Cheresh, Ph.D., Professor, Department of Immunology.

The work, "Disruption of Angiogenesis by PEX, a Noncatalytic Metalloproteinase Fragment with Integrin Binding Activity," by Peter C. Brooks, Steve Silleti, Tami L. von Schalscha, Martin Friedlander, and David A. Cheresh, is published in today's issue of Cell.

To grow and, ultimately, metastasize, malignant tumors must attract a rich blood supply to provide nourishment and remove wastes. In earlier studies, the Cheresh laboratory demonstrated that ang
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Contact: Robin B. Goldsmith
rgoldsmi@scripps.edu
(619) 784-8134
Scripps Research Institute
6-Feb-1998


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