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- W2056525439 abstract "Prostate cancer has become the most commonly diagnosed cancer in US men. 1 Boring CC Squires TS. Tong T Cancer statistics, 1992. CA-Cancer J Clin. 1992; 42: 19-38 Crossref PubMed Scopus (670) Google Scholar Today most prostate cancers from patients treated with androgen ablation progress from an androgen-dependent to an androgen-independent state. With the cloning of the androgen receptor cDNA 2 Chang CS Kokontis J Liao ST Molecular cloning of human and rat complementary DNA encoding androgen receptors. Science. 1988; 240: 324-326 Crossref PubMed Scopus (721) Google Scholar and the discovery that some mutant androgen receptors may be able to change steroid and antiandrogen specificity, 3 Taplin ME Bubley GJ Shuster TD et al. Mutation of the androgen-receptor gene in metastatic androgen-independent prostate cancer. N Engl J Med. 1995; 332: 1393-1398 Crossref PubMed Scopus (1021) Google Scholar the hypothesis that mutations in androgen receptors may be the reason why hydroxyflutamide, the active metabolite of flutamide, can activate androgen receptor target genes and stimulate (rather than inhibit) prostate cancer growth, is becoming widely accepted. The same mechanism has been used to explain the flutamide withdrawal syndrome, in which patients who experience an increase in prostate-specific antigen (PSA) while taking flutamide, have a decrease in PSA after withdrawal of treatment. Since this syndrome often heralds the failure of androgen-ablative therapy, elucidating the mechanism by which hydroxyflutamide increases the expression of PSA may provide a new approach to delaying or reversing the emergence of androgen independence." @default.
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- W2056525439 date "1997-03-01" @default.
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- W2056525439 title "Hydroxyflutamide may not always be a pure antiandrogen" @default.
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- W2056525439 doi "https://doi.org/10.1016/s0140-6736(05)61756-4" @default.
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