rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2007-12-31
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pubmed:abstractText |
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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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1532-6535
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
83
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
160-6
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pubmed:dateRevised |
2011-4-1
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pubmed:meshHeading |
pubmed-meshheading:17882159-Humans,
pubmed-meshheading:17882159-Breast Neoplasms,
pubmed-meshheading:17882159-Female,
pubmed-meshheading:17882159-Enzyme Inhibitors,
pubmed-meshheading:17882159-Genetic Variation,
pubmed-meshheading:17882159-Treatment Outcome,
pubmed-meshheading:17882159-Phenotype,
pubmed-meshheading:17882159-Patient Selection,
pubmed-meshheading:17882159-Biotransformation,
pubmed-meshheading:17882159-Pharmacogenetics,
pubmed-meshheading:17882159-Genotype,
pubmed-meshheading:17882159-Antineoplastic Agents, Hormonal
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