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Drug Inhibits Colon Cancer in Mice
Date:2/12/2009

Treated with enzastaurin, even tumors that did develop weren't as advanced, study finds

THURSDAY, Feb. 12 (HealthDay News) -- A drug called enzastaurin significantly reduced the development of colon cancer in mice, and tumors that did develop were less advanced and aggressive than those in mice that didn't receive the drug, according to a study by researchers at the Mayo Clinic in Florida.

The findings, coupled with the fact that the drug appears to have minimal side effects, suggest that enzastaurin might offer an effective chemopreventive treatment in people at high risk for colon cancer, the researchers said. The study is to be published in the Feb. 15 issue of the journal Cancer Research.

"There is a need for an agent that has a proven ability to reduce colon cancer risk, and this study suggests that enzastaurin could be uniquely effective," senior investigator Nicole Murray, of the department of cancer biology, said in a Mayo news release.

Enzastaurin is designed to suppress signaling through the PKC-beta pathway. In a previous study, the Mayo team found that the pathway is necessary for the start of colon cancer in mice exposed to a carcinogen.

"These mice develop tumors similar to tumors found in humans, but mice without the PKC-beta gene do not," Murray said.

In the new study, the Mayo researchers gave enzastaurin daily to one group of mice and then exposed them, as well as a control group of mice that didn't receive the drug, to a carcinogen that causes colon tumors.

After 22 weeks, 50 percent of the treated mice and 80 percent of the untreated mice had developed tumors. The tumors that did develop in the treated mice were not as advanced as those in the untreated mice.

Enzastaurin is currently being tested to treat a range of human cancers, including B-cell lymphoma and high-grade brain gliomas.

More information

The U.S. National Cancer Institute has more about colon cancer prevention.



-- Robert Preidt



SOURCE: Mayo Clinic, news release, Feb. 11, 2009


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