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Shedding Light Into a Murky Pool

Paul N. Hopkins, MD, MSPH; Eliot A. Brinton, MD

JAMA. 2003;290:2317-2319.

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

The article by Shearman et al¹ in this issue of THE JOURNAL brings intriguing genetic data to bear on several issues of considerable current controversy—the relationship between coronary artery disease (CAD) and estrogen action, the general utility of CAD associations with variants in candidate genes, and the challenges of identifying causative gene variants for common disease. In this interesting hybrid of a case-control and prospective design, the investigators extracted DNA from blood samples of a subset of unrelated members of the Framingham offspring cohort who were alive at examination 6 (approximately 27 years after the baseline examination). The subset was selected to achieve an approximately equal number of representative men and women from the cohort. The effects of several estrogen receptor (ESR1) gene variants were tested using primarily a case-control analysis in which offspring who had developed atherosclerotic disease . . . [Full Text of this Article]

Author Affiliations: Department of Cardiovascular Genetics, University of Utah, Salt Lake City).

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