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Views Of Tamoxifen And Synthetic Estrogen In Action Provide Clues For Designing Better Drugs

Medical Center and the Howard Hughes Medical Institute at the University of California at San Francisco have discovered the molecular mechanism by which tamoxifen blocks the effects of estrogen, a process that has been shown to prevent breast cancer in some women at high risk.

The results, published in the December 23 issue of Cell, provide valuable clues about ways to design new, more effective disease-preventing medications with fewer side effects.

"The goal is to figure out how to make drugs that retain the benefits of estrogen for brain, bone and heart and also have the benefits of estrogen blockers for the breast and uterus," said Geoffrey Greene, Ph.D., professor in the Ben May Institute of Cancer Research at the University of Chicago and a senior author of the study. "Now we have precise three-dimensional shapes of the complex that forms between several of these molecules and the estrogen receptor."

"These structural studies clarify how estrogens turn on genes and show precisely how tamoxifen blocks this process," said first-author Andrew Shiau, a graduate student in biochemistry & biophysics at UC San Francisco. "This sets the stage for intentional design of drugs with precise and selective action."

Estrogen has many health benefits. It delays the buildup of artery-clogging plaque, prevents bone loss leading to osteoporosis, and may even postpone the onset of Alzheimer's disease. These benefits disappear at menopause, when women stop making significant amounts of estrogen. Although taking replacement estrogen can restore these benefits, and prevent the hot flashes of menopause, continued exposure to this hormone increases a woman's risk of breast or uterine cancer.

Designer estrogens, also known as selective estrogen receptor modulators (SERMs), are a class of drugs that f
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Contact: John Easton
jeaston@mcis.bsd.uchicago.edu
773-702-6241
University of Chicago Medical Center
22-Dec-1998


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