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• W2334455588 abstract "The selective estrogen receptor modulator tamoxifen is approved for treatment of estrogen receptor-positive breast cancer in pre- and postmenopausal patients. The main active metabolite of tamoxifen is endoxifen, which has high affinity towards the receptor and reaches high plasma concentrations. Endoxifen results from cytochrome P450 enzyme CYP2D6 action. CYP2D6 is subject to genetic polymorphism, with a prevalence of enzyme deficiency of approximately 7% in most European populations. Enzyme deficiency is reliably predicted by genotyping of known CYP2D6 deficiency alleles. Poor metabolizers (homozygote carriers of deficiency alleles) exhibit lower endoxifen plasma concentrations. Retrospective analyses of tamoxifen study data according to CYP2D6 genotypes reveal a poorer oncological outcome for subjects with deficiency alleles in most studies (level 3 evidence). Data from randomized controlled studies (level 1 evidence) on the use of CYP2D6 typing for tamoxifen therapy are lacking. However, CYP2D6 genotyping before initiating tamoxifen therapy and avoidance of tamoxifen in postmenopausal women with a CYP2D6 enzyme deficiency seem warranted. Prescribing information does not list CYP2D6 status as a contraindication for tamoxifen. Pharmacological supression of hot flashes by comedication with CYP2D6 inhibitors (e.g., fluoxetine, paroxetine) must be avoided because such patients will become functional Poor metabolizers with lower endoxifen levels." @default.
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• W2334455588 date "2009-09-01" @default.
• W2334455588 modified "2023-09-25" @default.
• W2334455588 title "CYP2D6 and tamoxifen: pharmacogenetic reinvention of an established drug?1" @default.
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• W2334455588 doi "https://doi.org/10.1515/jlm.2009.048et" @default.
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