Finasteride metabolism and pharmacogenetics: new approaches to personalized prevention of prostate cancer

被引:4
|
作者
Hulin-Curtis, Sarah L. [1 ]
Petit, Dominique [1 ]
Figg, W. Douglas [2 ]
Hsing, Ann W. [3 ]
Reichardt, Juergen K. V. [1 ]
机构
[1] Univ Sydney, Bosch Inst, Camperdown, NSW, Australia
[2] NCI, Mol Pharmacol Sect, Med Oncol Branch, Bethesda, MD 20892 USA
[3] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA
关键词
androgen; CYP3A4; finasteride; haplotype; personalized medicine; pharmacogenetics; prostate cancer; single nucleotide polymorphism; SRD5A2; UGT1A; LIPID-LOWERING THERAPY; UDP-GLUCURONOSYLTRANSFERASES; CLINICAL PRESENTATION; AFRICAN-AMERICAN; GENETIC VARIANT; LINKAGE DISEQUILIBRIUM; ALLELIC VARIANTS; RISK; CYP3A4; IDENTIFICATION;
D O I
10.2217/FON.10.149
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Incidences of prostate cancer in most countries are increasing owing to better detection methods; however, prevention with the use of finasteride, a very effective steroid 5 alpha-reductase type II inhibitor, has been met with mixed success. A wide interindividual variation in response exists and is thought to be due to heritable factors. This article summarizes the literature that attempts to elucidate the molecular mechanisms of finasteride in terms of its metabolism, excretion and interaction with endogenous steroid molecules. We describe previously reported genetic variations of steroid-metabolizing genes and their potential association with finasteride efficacy. Based on the literature, we outline directions of research that may contribute to understanding the interindividual variation in finasteride prevention and to the future development of personalized medicine.
引用
收藏
页码:1897 / 1913
页数:17
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