© 2004 by Oxford University Press
© 2004 Oxford University Press
CORRESPONDENCE |
RESPONSE: Re: Active Tamoxifen Metabolite Plasma Concentrations After Coadministration of Tamoxifen and the Selective Serotonin Reuptake Inhibitor Paroxetine
Affiliations of authors: Division of Clinical Pharmacology, Indiana University School of Medicine, Indianapolis, IN (DAF, ZD); Breast Cancer Program, University of Michigan, Ann Arbor (JMR, DFH); and Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS); Lombardi Cancer Center, Georgetown University Medical Center, Washington, DC (MDJ, AN, PB)
Correspondence to: David A. Flockhart, MD, PhD, Division of Clinical Pharmacology, Indiana University School of Medicine, 1001 W. 10th St., Rm. OPD 320, Indianapolis, IN 46203 ( e-mail: dflockha@iupui.edu)
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We thank all three correspondents for their useful insights into our work. The data we presented demonstrate that the tamoxifen metabolite 4-hydroxy-N-desmethyl-tamoxifen (endoxifen) is equipotent to 4-hydroxy-tamoxifen in inhibiting estradiol-stimulated growth of MCF-7 cells (1) and that endoxifen concentrations were reduced in women who carried a genetic variant of CYP2D6 or in women with a wild-type CYP2D6 after coprescription with the CYP2D6 inhibitor paroxetine. The role of
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