1. Volume 65, Issue 1, Pages 30-36 (January 2014)
Enzalutamide in Castration-resistant Prostate Cancer Patients Progressing After Docetaxel and Abiraterone 
Andres Jan Schrader, Martin Boegemann, Carsten-H. Ohlmann, Thomas J. Schnoeller, Laura-Maria Krabbe, Turkan Hajili, Florian Jentzmik, Michael Stoeckle, Mark Schrader, Edwin Herrmann, Marcus V. Cronauer 
European Urology 
Volume 65, Issue 1, Pages (January 2014)
DOI: /j.eururo
Copyright © 2013 European Association of Urology Terms and Conditions

2. Fig. 1
Pathways involved in castration resistance of prostatic neoplasms. During hormonal therapy, most castration-resistant prostate cancer cells continue to depend on androgen receptor signaling but bypass the requirements for physiologic levels of circulating androgens. PCa=prostate cancer; CPRC=castration-resistant prostate cancer; AR=androgen receptor; LBD=ligand-binding domain; RTK=receptor tyrosine kinase.
European Urology  , 30-36DOI: ( /j.eururo )
Copyright © 2013 European Association of Urology Terms and Conditions

3. Fig. 2
Waterfall plot showing the maximum percentage reduction of prostate-specific antigen from baseline in 35 evaluable patients who received abiraterone and subsequent enzalutamide. PSA=prostate-specific antigen.
European Urology  , 30-36DOI: ( /j.eururo )
Copyright © 2013 European Association of Urology Terms and Conditions

4. Fig. 3
Overall survival (Kaplan-Meier estimate) of castration-, docetaxel-, and abiraterone-resistant patients receiving enzalutamide. The 6-mo overall survival rate was 65.1% and 90.0% for those patients who achieved a <50% and >50% prostate-specific antigen decrease, respectively, while taking enzalutamide (p=0.052; log-rank test). PSA=prostate-specific antigen.
European Urology  , 30-36DOI: ( /j.eururo )
Copyright © 2013 European Association of Urology Terms and Conditions

5. Fig. 4
Simplified model summarizing all currently known androgen receptor (AR)-dependent mechanisms involved in abiraterone and/or enzalutamide resistance of castration-resistant prostate cancer cells. However, the fact that promiscuous AR mutations and ARΔLBD are not mutually exclusive [14] reveals a more complex interplay between the different resistance mechanisms. LBD=ligand-binding domain.
European Urology  , 30-36DOI: ( /j.eururo )
Copyright © 2013 European Association of Urology Terms and Conditions