Salve From Serpents? UD Studies May Explain Why Viper-Venom Protein Stops Tumor Spread In Mice

To view vipers, molecules and McLane, go to http://www.udel.edu/PR/NewsReleases/Viper/viper.html

Viper snakes can kill, but a protein in their venom prevents the spread of tumors in laboratory mice, and a molecular 'portrait' now under development may explain why, according to a University of Delaware scientist profiled in the new issue of Cardiology Today, mailed Feb. 4.

Venom from Macmahon's Viper (Eristocophis macmahoni), found in Afghanistan and Pakistan, contains the protein, eristostatin, which blocks the "metastasis" or spread of tumors in mice injected with cancer cells, notes Mary Ann McLane, an assistant professor in UD's Department of Medical Technology. Her studies of eristostatin's structure, though preliminary, could help pharmaceutical companies develop cancer-fighting drugs, says McLane's collaborator, Stefan Niewiarowski of Temple University Medical School's Department of Physiology and Sol Sherry Thrombosis Research Center.

"The next step," McLane says, "is to find out exactly what it is about the structure of eristostatin that gives it this exciting capability in mice." With UD colleague Mary E. Miele, an assistant professor of medical technology, McLane also plans to study eristostatin's effect on metastatic melanoma cells.

Eristostatin is one of many viper-venom "disintegrins"--proteins that interact with a family of cellular receptors called integrins, McLane explains. Disintegrins are "potent inhibitors of platelet aggregation and cell adhesion," and therefore prevent an early step in blood clotting, Niewiarowski says. Once injected into a victim's bloodstream, disintegrins from viper-snake venom stop the sticky protein, fibrinogen, from binding with platelets. The global quest to better understand disintegrins, launched in the late 1980s, already has resulted in a commercially a

Contact: Ginger Pinholster
University of Delaware

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