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Adele L. Franks, MD; Karen K. Steinberg, PhD

JAMA. 1999;281:2243-2244.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

The discovery that pharmacologic agents can be estrogenic in some tissues while antiestrogenic in others has led to intense interest in better understanding the mechanism by which molecular structure interacts with cellular receptors to selectively affect DNA transcription in different organs. Appreciation for these selective estrogen receptor modulators (SERMs) has inevitably given way to the hope of developing one that could confer all of the benefits of estrogen without any of its risks. The first widely used SERM, tamoxifen citrate, has been found to have the antiestrogenic effect of reducing risk for breast cancer as well as beneficial estrogenic effects on serum lipids and bone density in women.¹ However, tamoxifen also has the undesirable antiestrogenic effect of causing hot flashes and the undesirable estrogenic effects of increasing risk for endometrial cancer and venous thromboembolism in women.¹ Because raloxifene hydrochloride, a second-generation SERM, . . . [Full Text of this Article]

Author Affiliations: The Prudential Center for Health Care Research (Dr Franks) and Molecular Biology Branch, Centers for Disease Control and Prevention (Dr Steinberg), Atlanta, Ga.

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