Washington, D.C Researchers at Georgetown University's Lombardi Comprehensive Cancer Center have decoded the step-by-step process by which a class of popular anti-diabetes drugs inhibits cancerous tumor growth. With the discovery of this molecular chain of events, as reported in the September 2003 issue of Molecular and Cellular Biology, the Georgetown researchers are now studying whether these anti-diabetes drugs, called glitazones, could one day be effective anti-cancer drugs.

Glitazones are taken by more than two million people with Type 2 diabetes. They are marketed under the names AvandiaTM and ActosTM, by SmithKline Beecham and Eli Lilly, respectively. Glitazones bind to a particular target on a cell, and in diabetics, they work by reducing insulin resistance at the sites of insulin action in the muscle and liver. Previous studies have also shown that glitazones also have the ability to inhibit tumor growth. However, until this study no one understood how this process worked.

"This study shows for the first time a direct link between a gene causing breast and other cancers and a gene linked to diabetes and the production of fat cells," said Richard Pestell, M.D., PhD, director of Lombardi Comprehensive Cancer Center. "The link between these cellular components may be a lynchpin in some cancers linking some cancers and metabolism directly. Potentially, we could be on the way to finding new therapeutic leads that would improve both diseases."

Pestell and his colleagues describe a complex relationship between a cancer causing gene, Cyclin D1, and a cancer-blocking receptor called PPAR gamma, which is involved in fat cell development. They are respectively found in breast cancer tissue and normal breast tissue. When PPAR is "turned on" by glitazones, tumor growth is inhibited. Conversely, when Cyclin D1 is activated in cells, it causes cancer cells to divide uncontrollably and excessively. <
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Contact: Elizabeth McDonald
eem6@georgetown.edu
202-687-5100
Georgetown University Medical Center
15-Sep-2003

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