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- W2016380091 abstract "Death from prostate cancer is invariably due to metastatic dissemination and resistance to androgen deprivation therapy, the definition of castration-resistant prostate cancer (CRPC). During the last decade, we dramatically changed ourminds concerning the old paradigm that stated prostate cancer is chemoresistant but hormone sensitive for about 2 yr and then becomes hormone refractory with a dismal life expectancy of about 1 yr. Until very recently, only docetaxel-based chemotherapy was shown to modestly improve survival since the identification of therapeutic castration by Huggins in 1941 [1,2]. One of the major pillars of the new paradigm is a better understanding of molecular alterations involved in prostate cancer progression. The molecular basis of the development ofCRPC ismainly the activationof theandrogen receptor (AR) axis via multiple pathways including (1) activation of the AR by nonsteroids such as growth factors and cytokines via deregulation of multiple oncogenic signalling pathways, (2) an increase in intratumour androgen levels and/or alteration in the AR structure, and (3) the involvement of alternative pathways such as the activation of the PI3K or the MET pathway [3]. Based on this rationale, a new generation of hormonal manipulations such as androgen biosynthesis inhibitors (CYP17 inhibitors such as acetate abiraterone) or AR antagonists (eg, enzalutamide) yielded very promising anddramatic antitumouractivity inearlyphase1and2 trials. Both agents have yielded an overall survival benefit in the postdocetaxel setting and radiographic progression-free survival in the predocetaxel setting; enzalutamide was also" @default.
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- W2016380091 date "2014-10-01" @default.
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- W2016380091 title "One Size Does Not Fit All: Can We Choose the Best Sequence of Treatment in Asymptomatic Castration-resistant Prostate Cancer Patients?" @default.
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- W2016380091 doi "https://doi.org/10.1016/j.eururo.2014.03.024" @default.
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