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Purdue scientists: To stop cancer, keep your Icmt away from your Ras

ffect growth commands. So Gibbs and Hrycyna's labs joined forces to block the biochemical activity of Icmt with small drug molecules, preventing the methyl esterification of Ras and effectively breaking its ability to localize to the plasma membrane.

"This effort depended on both labs," Anderson said. "The Gibbs laboratory brought synthetic expertise, and the Hrycyna laboratory brought large quantities of the protein and the expertise to assay the effects of the inhibitors."

Other groups have shown recently that this lack of a methyl cap causes Ras to localize in the wrong region of the cell and, importantly, results in a Ras protein that cannot support cancerous growth.

"These findings are terrific news for our efforts," said Hrycyna. "If our inhibitor molecules directed at stopping or slowing the activity of Icmt in tumor cells are effective, we should be able to stop the growth of Ras-based cancers."

Hrycyna said she believed the discovery could ultimately throw a wrench into cancer's operation, but that it was still too early to predict victory.

"We have succeeded in stopping Ras at the protein level and are just beginning to work with whole cells," she said. "This is very different from getting results in animals, and we're still a long way from human trials. No one should look for this to cure cancer anytime soon, though we are extremely encouraged by these initial results."

But to move the process toward the goal of curing cancer, the group plans to look into other ways of altering Icmt to increase the effect.

"Other ways of changing Icmt might make it even more potent at stopping the development of Ras," Henriksen said. "We'd like to look at all our options and combine them into the most potent inhibitor we can manage - that's a good goal for the near future."


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Contact: Chad Boutin
cboutin@purdue.edu
765-494-2081
Purdue University
28-Mar-2004


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