Abstract
Tamoxifen continues to be a standard endocrine therapy for the prevention and treatment of estrogen receptor (ER)-positive breast cancer. Tamoxifen can be considered a classic "pro-drug," requiring metabolic activation to elicit pharmacological activity. CYP2D6 is the rate-limiting enzyme catalyzing the conversion of tamoxifen into metabolites with significantly greater affinity for the ER and greater ability to inhibit cell proliferation. Both genetic and environmental (drug-induced) factors that alter CYP2D6 enzyme activity directly affect the concentrations of the active tamoxifen metabolites and the outcomes of patients receiving adjuvant tamoxifen. The a priori knowledge of the pharmacogenetic variation known to abrogate CYP2D6 enzyme activity may provide a means by which the hormonal therapy of breast cancer can be individualized.
Original language | English (US) |
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Pages (from-to) | 160-166 |
Number of pages | 7 |
Journal | Clinical pharmacology and therapeutics |
Volume | 83 |
Issue number | 1 |
DOIs | |
State | Published - Jan 9 2008 |
ASJC Scopus subject areas
- Pharmacology
- Pharmacology (medical)