LOS ANGELES, CA (August 12, 2002) In recent years, laboratory discoveries have led to the development of new drugs designed to target and attack cancer cells, leaving healthy ones intact. One key weapon in this arsenal of new therapies is called Herceptin, a drug that is currently used to treat breast cancer and works by targeting a specific protein that controls cell growth called HER-2/neu. But despite the drug's effectiveness, tumors shrink in only the small percentage of breast cancer patients whose cancer cells express an over-abundance of HER-2/neu.

Now, laboratory studies conducted by researchers at Cedars-Sinai Medical Center and Genentech have found that a potent experimental drug called 2C4 slows tumor growth in both breast and prostate cancer tumors in mice even when small amounts of HER-2/neu are expressed. The findings appear in the August issue of the journal, Cancer Cell, and may lead to a new way to treat breast and prostate cancers and other solid tumors.

"We found that 2C4 not only targeted HER-2/neu, but that it disrupted cell signaling among the entire HER family of proteins," said Dr. David Agus, Research Director at the Cedars-Sinai Prostate Cancer Center and first author of the study. "As a result of these lab studies, clinical trials are currently underway to test the safety and effectiveness of 2C4 in patients with breast and prostate cancer, as well as other solid tumors."

The drug, called 2C4, is a monoclonal antibody, or molecule that enlists the body's immune system to attack foreign invaders, such as viruses or bacteria. Produced by Genentech, Inc., 2C4 is similar to Herceptin in that it targets HER-2/neu, a member of the HER kinase family of proteins. The protein sits on the surface of cancer cells and receives signals from "growth factor" molecules within the HER family, which, in turn, stimulate tumors to grow.

"Although HER-2/neu is a major target because it plays an important role in tumor
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Contact: Kelli Stauning
kelli.stauning@cshs.org
310-423-3674
Cedars-Sinai Medical Center
12-Aug-2002

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