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Comment
. 2010 Sep 1;16(17):4308-10.
doi: 10.1158/1078-0432.CCR-10-1506. Epub 2010 Jul 22.

Personalized tamoxifen: a step closer but miles to go

Aditya Bardia  1 , Vered Stearns
Affiliations
Comment

Personalized tamoxifen: a step closer but miles to go

Aditya Bardia et al. Clin Cancer Res. .

Abstract

Genetic variants in CYP2D6 lead to reduced conversion of tamoxifen to the active metabolite endoxifen. However, the role of the CYP2D6 genotype in predicting tamoxifen-associated outcomes remains controversial. Accurate assignment of the CYP2D6 genotype in archival tissues is crucial for future studies attempting to determine risk prediction of outcomes in tamoxifen-treated individuals.

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Figures

Figure 1
Figure 1
Examples of the inter-relationship between host, tumor, and environmental factors (pharmaco-epi-bio-genomic triad) that determine the response to tamoxifen in an individual patient (phenotype). A. Variants in genes encoding for enzymes can influence metabolism and elimination of tamoxifen (host genetic factors). B. Differences in estrogen pathway may predict sensitivity or resistance to tamoxifen and its antiestrogenic metabolites in tumor cell and its inhibition by tamoxifen metabolites (tumor biology factors). C. Environmental factors that can influence tamoxifen response. Abbreviations: Co A = Co-activator ER = Estrogen Receptor ERE = Estrogen Response Element HER2 = Human Epidermal Growth Factor 2 IGFR = Insulin Growth Factor Receptor
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Comment on

References

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    1. Stearns V, Johnson MD, Rae JM, et al. Active tamoxifen metabolite plasma concentrations after coadministration of tamoxifen and the selective serotonin reuptake inhibitor paroxetine. J Natl Cancer Inst. 2003;95:1758–1764. - PubMed
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    1. Bardia A, Stearns V. Pharmacogenomics of Tamoxifen: Ready for Prime Time? Current Breast Cancer Reports. 2010;2:32–41.

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