CYP2D6 Genotype, Antidepressant Use, and Tamoxifen Metabolism During Adjuvant Breast Cancer Treatment
Background: The efficacy of tamoxifen therapy for the treatment of breast cancer varies widely among individuals. Plasma concentrations of the active tamoxifen metabolite endoxifen are associated with the cytochrome P450 (CYP) 2D6 genotype. We examined the effects of concomitant use of selective ser...
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| Published in | JNCI : Journal of the National Cancer Institute Vol. 97; no. 1; pp. 30 - 39 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Cary, NC
Oxford University Press
05.01.2005
Oxford Publishing Limited (England) |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0027-8874 1460-2105 1460-2105 |
| DOI | 10.1093/jnci/dji005 |
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| Abstract | Background: The efficacy of tamoxifen therapy for the treatment of breast cancer varies widely among individuals. Plasma concentrations of the active tamoxifen metabolite endoxifen are associated with the cytochrome P450 (CYP) 2D6 genotype. We examined the effects of concomitant use of selective serotonin reuptake inhibitor antidepressants, which are CYP2D6 enzyme inhibitors commonly prescribed to treat hot flashes in women who take tamoxifen, and genotypes for genes that encode tamoxifen-metabolizing enzymes on plasma concentrations of tamoxifen and its metabolites. Methods: Eighty patients with newly diagnosed with breast cancer who were beginning tamoxifen therapy (20 mg/day orally), 24 of whom were taking CYP2D6 inhibitors, were genotyped for common alleles of the CYP2D6, CYP2C9, CYP3A5, and sulfotransferase (SULT) 1A1 genes. Plasma concentrations of tamoxifen and its metabolites were measured after 1 and 4 months of tamoxifen therapy. Differences in plasma concentrations of tamoxifen and its metabolites between genotype groups were analyzed by the Wilcoxon rank sum test. All statistical tests were two-sided. Results: Among all women, plasma endoxifen concentrations after 4 months of tamoxifen therapy were statistically significantly lower in subjects with a CYP2D6 homozygous variant genotype (20.0 nM, 95% confidence interval [CI] = 11.1 to 28.9 nM) or a heterozygous genotype (43.1 nM, 95% CI = 33.3 to 52.9 nM) than in those with a homozygous wild-type genotype (78.0 nM, 95%CI = 65.9 to 90.1 nM) (both P = .003). Among subjects who carried a homozygous wild-type genotype, the mean plasma endoxifen concentration for those who were using CYP2D6 inhibitors was 58% lower than that for those who were not (38.6 nM versus 91.4 nM, difference = –52.8 nM, 95% CI = –86.1 to –19.5 nM, P = .0025). The plasma endoxifen concentration was slightly reduced in women taking venlafaxine, a weak inhibitor of CYP2D6, whereas the plasma endoxifen concentration was reduced substantially in subjects who took paroxetine (a potent inhibitor of CYP2D6). Genetic variations of CYP2C9, CYP3A5, or SULT1A1 had no statistically significant associations with plasma concentrations of tamoxifen or its metabolites. Conclusion: Interactions between CYP2D6 polymorphisms and coadministered antidepressants and other drugs that are CYP2D6 inhibitors may be associated with altered tamoxifen activity. |
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| AbstractList | BACKGROUND: The efficacy of tamoxifen therapy for the treatment of breast cancer varies widely among individuals. Plasma concentrations of the active tamoxifen metabolite endoxifen are associated with the cytochrome P450 (CYP) 2D6 genotype. We examined the effects of concomitant use of selective serotonin reuptake inhibitor antidepressants, which are CYP2D6 enzyme inhibitors commonly prescribed to treat hot flashes in women who take tamoxifen, and genotypes for genes that encode tamoxifen-metabolizing enzymes on plasma concentrations of tamoxifen and its metabolites. METHODS: Eighty patients with newly diagnosed with breast cancer who were beginning tamoxifen therapy (20 mg/day orally), 24 of whom were taking CYP2D6 inhibitors, were genotyped for common alleles of the CYP2D6, CYP2C9, CYP3A5, and sulfotransferase (SULT) 1A1 genes. Plasma concentrations of tamoxifen and its metabolites were measured after 1 and 4 months of tamoxifen therapy. Differences in plasma concentrations of tamoxifen and its metabolites between genotype groups were analyzed by the Wilcoxon rank sum test. All statistical tests were two-sided. RESULTS: Among all women, plasma endoxifen concentrations after 4 months of tamoxifen therapy were statistically significantly lower in subjects with a CYP2D6 homozygous variant genotype (20.0 nM, 95% confidence interval [CI] = 11.1 to 28.9 nM) or a heterozygous genotype (43.1 nM, 95% CI = 33.3 to 52.9 nM) than in those with a homozygous wild-type genotype (78.0 nM, 95%CI = 65.9 to 90.1 nM) (both P = .003). Among subjects who carried a homozygous wild-type genotype, the mean plasma endoxifen concentration for those who were using CYP2D6 inhibitors was 58% lower than that for those who were not (38.6 nM versus 91.4 nM, difference = -52.8 nM, 95% CI = -86.1 to -19.5 nM, P = .0025). The plasma endoxifen concentration was slightly reduced in women taking venlafaxine, a weak inhibitor of CYP2D6, whereas the plasma endoxifen concentration was reduced substantially in subjects who took paroxetine (a potent inhibitor of CYP2D6). Genetic variations of CYP2C9, CYP3A5, or SULT1A1 had no statistically significant associations with plasma concentrations of tamoxifen or its metabolites. CONCLUSION: Interactions between CYP2D6 polymorphisms and coadministered antidepressants and other drugs that are CYP2D6 inhibitors may be associated with altered tamoxifen activity. The efficacy of tamoxifen therapy for the treatment of breast cancer varies widely among individuals. Plasma concentrations of the active tamoxifen metabolite endoxifen are associated with the cytochrome P450 (CYP) 2D6 genotype. We examined the effects of concomitant use of selective serotonin reuptake inhibitor antidepressants, which are CYP2D6 enzyme inhibitors commonly prescribed to treat hot flashes in women who take tamoxifen, and genotypes for genes that encode tamoxifen-metabolizing enzymes on plasma concentrations of tamoxifen and its metabolites. Eighty patients with newly diagnosed with breast cancer who were beginning tamoxifen therapy (20 mg/day orally), 24 of whom were taking CYP2D6 inhibitors, were genotyped for common alleles of the CYP2D6, CYP2C9, CYP3A5, and sulfotransferase (SULT) 1A1 genes. Plasma concentrations of tamoxifen and its metabolites were measured after 1 and 4 months of tamoxifen therapy. Differences in plasma concentrations of tamoxifen and its metabolites between genotype groups were analyzed by the Wilcoxon rank sum test. All statistical tests were two-sided. Among all women, plasma endoxifen concentrations after 4 months of tamoxifen therapy were statistically significantly lower in subjects with a CYP2D6 homozygous variant genotype (20.0 nM, 95% confidence interval [CI] = 11.1 to 28.9 nM) or a heterozygous genotype (43.1 nM, 95% CI = 33.3 to 52.9 nM) than in those with a homozygous wild-type genotype (78.0 nM, 95%CI = 65.9 to 90.1 nM) (both P = .003). Among subjects who carried a homozygous wild-type genotype, the mean plasma endoxifen concentration for those who were using CYP2D6 inhibitors was 58% lower than that for those who were not (38.6 nM versus 91.4 nM, difference = -52.8 nM, 95% CI = -86.1 to -19.5 nM, P = .0025). The plasma endoxifen concentration was slightly reduced in women taking venlafaxine, a weak inhibitor of CYP2D6, whereas the plasma endoxifen concentration was reduced substantially in subjects who took paroxetine (a potent inhibitor of CYP2D6). Genetic variations of CYP2C9, CYP3A5, or SULT1A1 had no statistically significant associations with plasma concentrations of tamoxifen or its metabolites. Interactions between CYP2D6 polymorphisms and coadministered antidepressants and other drugs that are CYP2D6 inhibitors may be associated with altered tamoxifen activity. The efficacy of tamoxifen therapy for the treatment of breast cancer varies widely among individuals. Plasma concentrations of the active tamoxifen metabolite endoxifen are associated with the cytochrome P450 (CYP) 2D6 genotype. We examined the effects of concomitant use of selective serotonin reuptake inhibitor antidepressants, which are CYP2D6 enzyme inhibitors commonly prescribed to treat hot flashes in women who take tamoxifen, and genotypes for genes that encode tamoxifen-metabolizing enzymes on plasma concentrations of tamoxifen and its metabolites.BACKGROUNDThe efficacy of tamoxifen therapy for the treatment of breast cancer varies widely among individuals. Plasma concentrations of the active tamoxifen metabolite endoxifen are associated with the cytochrome P450 (CYP) 2D6 genotype. We examined the effects of concomitant use of selective serotonin reuptake inhibitor antidepressants, which are CYP2D6 enzyme inhibitors commonly prescribed to treat hot flashes in women who take tamoxifen, and genotypes for genes that encode tamoxifen-metabolizing enzymes on plasma concentrations of tamoxifen and its metabolites.Eighty patients with newly diagnosed with breast cancer who were beginning tamoxifen therapy (20 mg/day orally), 24 of whom were taking CYP2D6 inhibitors, were genotyped for common alleles of the CYP2D6, CYP2C9, CYP3A5, and sulfotransferase (SULT) 1A1 genes. Plasma concentrations of tamoxifen and its metabolites were measured after 1 and 4 months of tamoxifen therapy. Differences in plasma concentrations of tamoxifen and its metabolites between genotype groups were analyzed by the Wilcoxon rank sum test. All statistical tests were two-sided.METHODSEighty patients with newly diagnosed with breast cancer who were beginning tamoxifen therapy (20 mg/day orally), 24 of whom were taking CYP2D6 inhibitors, were genotyped for common alleles of the CYP2D6, CYP2C9, CYP3A5, and sulfotransferase (SULT) 1A1 genes. Plasma concentrations of tamoxifen and its metabolites were measured after 1 and 4 months of tamoxifen therapy. Differences in plasma concentrations of tamoxifen and its metabolites between genotype groups were analyzed by the Wilcoxon rank sum test. All statistical tests were two-sided.Among all women, plasma endoxifen concentrations after 4 months of tamoxifen therapy were statistically significantly lower in subjects with a CYP2D6 homozygous variant genotype (20.0 nM, 95% confidence interval [CI] = 11.1 to 28.9 nM) or a heterozygous genotype (43.1 nM, 95% CI = 33.3 to 52.9 nM) than in those with a homozygous wild-type genotype (78.0 nM, 95%CI = 65.9 to 90.1 nM) (both P = .003). Among subjects who carried a homozygous wild-type genotype, the mean plasma endoxifen concentration for those who were using CYP2D6 inhibitors was 58% lower than that for those who were not (38.6 nM versus 91.4 nM, difference = -52.8 nM, 95% CI = -86.1 to -19.5 nM, P = .0025). The plasma endoxifen concentration was slightly reduced in women taking venlafaxine, a weak inhibitor of CYP2D6, whereas the plasma endoxifen concentration was reduced substantially in subjects who took paroxetine (a potent inhibitor of CYP2D6). Genetic variations of CYP2C9, CYP3A5, or SULT1A1 had no statistically significant associations with plasma concentrations of tamoxifen or its metabolites.RESULTSAmong all women, plasma endoxifen concentrations after 4 months of tamoxifen therapy were statistically significantly lower in subjects with a CYP2D6 homozygous variant genotype (20.0 nM, 95% confidence interval [CI] = 11.1 to 28.9 nM) or a heterozygous genotype (43.1 nM, 95% CI = 33.3 to 52.9 nM) than in those with a homozygous wild-type genotype (78.0 nM, 95%CI = 65.9 to 90.1 nM) (both P = .003). Among subjects who carried a homozygous wild-type genotype, the mean plasma endoxifen concentration for those who were using CYP2D6 inhibitors was 58% lower than that for those who were not (38.6 nM versus 91.4 nM, difference = -52.8 nM, 95% CI = -86.1 to -19.5 nM, P = .0025). The plasma endoxifen concentration was slightly reduced in women taking venlafaxine, a weak inhibitor of CYP2D6, whereas the plasma endoxifen concentration was reduced substantially in subjects who took paroxetine (a potent inhibitor of CYP2D6). Genetic variations of CYP2C9, CYP3A5, or SULT1A1 had no statistically significant associations with plasma concentrations of tamoxifen or its metabolites.Interactions between CYP2D6 polymorphisms and coadministered antidepressants and other drugs that are CYP2D6 inhibitors may be associated with altered tamoxifen activity.CONCLUSIONInteractions between CYP2D6 polymorphisms and coadministered antidepressants and other drugs that are CYP2D6 inhibitors may be associated with altered tamoxifen activity. |
| Author | Rae, James M. Ward, Bryan Weinshilboum, Richard M. Ullmer, Lynda Lemler, Suzanne Hayden, Jill Araba, Adjei Hayes, Daniel F. Lee, Kyung-Hoon Storniolo, Anna Maria Jin, Yan Stearns, Vered Skaar, Todd Nguyen, Anne Flockhart, David A. Li, Lang Desta, Zeruesenay Ho, Herbert Blanchard, Rebecca |
| Author_xml | – sequence: 1 givenname: Yan surname: Jin fullname: Jin, Yan organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 2 givenname: Zeruesenay surname: Desta fullname: Desta, Zeruesenay organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 3 givenname: Vered surname: Stearns fullname: Stearns, Vered organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 4 givenname: Bryan surname: Ward fullname: Ward, Bryan organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 5 givenname: Herbert surname: Ho fullname: Ho, Herbert organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 6 givenname: Kyung-Hoon surname: Lee fullname: Lee, Kyung-Hoon organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 7 givenname: Todd surname: Skaar fullname: Skaar, Todd organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 8 givenname: Anna Maria surname: Storniolo fullname: Storniolo, Anna Maria organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 9 givenname: Lang surname: Li fullname: Li, Lang organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 10 givenname: Adjei surname: Araba fullname: Araba, Adjei organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 11 givenname: Rebecca surname: Blanchard fullname: Blanchard, Rebecca organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 12 givenname: Anne surname: Nguyen fullname: Nguyen, Anne organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 13 givenname: Lynda surname: Ullmer fullname: Ullmer, Lynda organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 14 givenname: Jill surname: Hayden fullname: Hayden, Jill organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 15 givenname: Suzanne surname: Lemler fullname: Lemler, Suzanne organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 16 givenname: Richard M. surname: Weinshilboum fullname: Weinshilboum, Richard M. organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 17 givenname: James M. surname: Rae fullname: Rae, James M. organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 18 givenname: Daniel F. surname: Hayes fullname: Hayes, Daniel F. organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) – sequence: 19 givenname: David A. surname: Flockhart fullname: Flockhart, David A. organization: Affiliation of authors: Division of Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN (YJ, ZD, BW, HH, KHL, TS, AMS, LL, AN, DAF); Breast Cancer Program, University of Michigan, Ann Arbor, MI (LU, JMR, JH, JMR, DFH); Department of Pharmacology, Mayo Clinic, Rochester, MN (AA, RMW); Breast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD (VS);Fox Chase Cancer Center, Philadelphia, PA (RB) |
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| Keywords | Antineoplastic agent Human Genetic variability Enzyme Isozyme Serotonin antagonist Cytochrome P450 Antiestrogen Adjuvant treatment Genotype Breast cancer Antihormone Malignant tumor Metabolism Tamoxifene Mammary gland diseases Chemotherapy Cancerology Antidepressant agent Pharmacokinetics Non steroid compound Polymorphism |
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| Notes | Correspondence to: David A. Flockhart, MD, PhD, Division of Clinical Pharmacology, Indiana University, School of Medicine, 1001 W. 10th St., W. D. Myers Building, W7123, Indianapolis, IN 46202 (e-mail: dflockha@iupui.edu) istex:5ECA15411E94F644C9DE666D130BFB33EB18E4C2 ark:/67375/HXZ-C556KXNH-M local:0005 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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| Title | CYP2D6 Genotype, Antidepressant Use, and Tamoxifen Metabolism During Adjuvant Breast Cancer Treatment |
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