Journal
CLINICAL PHARMACOLOGY & THERAPEUTICS
Volume 83, Issue 1, Pages 160-166Publisher
WILEY
DOI: 10.1038/sj.clpt.6100367
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Funding
- NATIONAL CANCER INSTITUTE [K12CA090628, P50CA116201, P30CA015083] Funding Source: NIH RePORTER
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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.
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