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Tamoxifen pharmacogenomics: the role of CYP2D6 as a predictor of drug response.

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.[1]

References

  1. Tamoxifen pharmacogenomics: the role of CYP2D6 as a predictor of drug response. Goetz, M.P., Kamal, A., Ames, M.M. Clin. Pharmacol. Ther. (2008) [Pubmed]
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