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Diabetes drug may be new tool in treating breast cancer

p>The new study reports that the anti-tumor effects of the PPAR gamma receptor are actually controlled by the cancer-causing Cyclin D1. In short, too much Cyclin D1 trumps the PPAR gamma receptor, turning off its ability to inhibit tumor growth.

Based on these findings, the Georgetown researchers believe that reduction in PPAR expression coupled with the increase in Cyclin D1 may represent a key genetic alteration underlying the transition from normal breast tissue to breast cancer. These findings suggest that drugs that block the effects of Cyclin D1 may be useful in stopping the conversion of normal tissue to malignant tissue.

The discoverer of the human Cyclin D1 gene, Andrew Arnold, M.D., professor and Director of the Center for Molecular Medicine at the University of Connecticut School of Medicine, agrees with the Georgetown researchers.

"This link between Cyclin D1 and PPAR gamma biochemical pathways is fascinating and clearly worthy of further exploration, including the potential for yielding new treatment modalities for cancer," said Dr. Arnold.

The study published in Molecular and Cellular Biology was funded by the National Cancer Institute.


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Contact: Elizabeth McDonald
eem6@georgetown.edu
202-687-5100
Georgetown University Medical Center
15-Sep-2003


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