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- W2152364190 abstract "Abstract Various molecular mechanisms have been implicated in the progression from hormone-sensitive to castration-resistant prostate cancer (CRPC). Novel targeted agents to treat CRPC have been developed that inhibit either androgen receptor (AR)-mediated signaling (AR antagonists and inhibitors of androgen synthesis) or non–AR-mediated signaling (inhibitors of Src, mammalian target of rapamycin, chaperone proteins, insulin-like growth factor-1 receptor, vascular endothelial growth factor, and endothelin-A receptor) pathways. However, variable efficacy has been observed in clinical trials, most likely because of the biologic heterogeneity of CRPC. To account for potential differences in disease biology, a more individualized approach to treatment, based on genomic and/or proteomic analyses of individual tumors, is being investigated. By identifying tumors with a characteristic molecular subtype and assigning treatment accordingly, it is hoped that a higher proportion of patients will benefit from targeted therapy. Additionally, lessons learned through the application of these technologies to prostate cancer may subsequently influence therapeutic development in other solid tumors." @default.
- W2152364190 created "2016-06-24" @default.
- W2152364190 creator A5012804612 @default.
- W2152364190 creator A5081123075 @default.
- W2152364190 date "2011-02-21" @default.
- W2152364190 modified "2023-10-18" @default.
- W2152364190 title "Castration-Resistant Prostate Cancer: Targeted Therapies and Individualized Treatment" @default.
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- W2152364190 doi "https://doi.org/10.1634/theoncologist.2010-0216" @default.
- W2152364190 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3228103" @default.
- W2152364190 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21339259" @default.
- W2152364190 hasPublicationYear "2011" @default.
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