Enzalutamide in castration-resistant prostate cancer patients with visceral disease in the liver and/or lung: Outcomes from the randomized controlled phase 3 AFFIRM trial.
de Bono, JS
MetadataShow full item record
Background Patients with metastatic castration-resistant prostate cancer (mCRPC) and visceral metastases have a worse prognosis than those with nonvisceral metastases. Treatment with the androgen receptor inhibitor enzalutamide in the phase 3 AFFIRM trial led to significant improvements in outcomes for patients with mCRPC. For the current report, the authors analyzed the efficacy of enzalutamide among patients from the AFFIRM trial who had visceral disease.Methods Patients who had liver and/or lung metastases at baseline were selected for prespecified overall survival (OS) and exploratory post hoc analyses, including prostate-specific antigen (PSA) response and the time to PSA and radiographic progression.Results In patients who had liver metastases (n = 92), enzalutamide was associated with a lower risk of radiographic progression (hazard ratio [HR], 0.645; 95% confidence interval [CI], 0.413-1.008), improved 12-month OS (37.7% vs 20.6%) and radiographic progression-free survival (rPFS) (11.6% vs 3.0%) rates, and higher PSA response rates (35.1% vs 4.8%) compared with placebo. Enzalutamide-treated patients who had lung metastases (n = 104) had improved median OS (HR, 0.848; 95% CI, 0.510-1.410), a substantially reduced risk of radiographic progression (HR, 0.386; 95% CI, 0.259-0.577), improved 12-month OS (65.1% vs 55.3%) and rPFS (30.9% vs 8.2%) rates, increased time to PSA progression (HR, 0.358; 95% CI, 0.204-0.627), and a better PSA response rate (52.1% vs 4.9%) compared with those who received placebo. No increase in treatment-related adverse events was observed for the visceral metastases cohort compared with the nonvisceral metastases cohort.Conclusions Across multiple endpoints, patients who have visceral metastases have better outcomes with enzalutamide than with placebo. Cancer 2017;123:253-262. © 2016 American Cancer Society.
Version of record
Proportional Hazards Models
Prostatic Neoplasms, Castration-Resistant
Prostate Cancer Targeted Therapy Group
License start date
Cancer, 2017, 123 (2), pp. 253 - 262
Showing items related by title, author, creator and subject.
EFSUMB guidelines and recommendations on the clinical use of ultrasound elastography. Part 2: Clinical applications. Cosgrove, D; Piscaglia, F; Bamber, J; Bojunga, J; Correas, J-M; Gilja, OH; Klauser, AS; Sporea, I; Calliada, F; Calliada, F; Cantisani, V; D'Onofrio, M; Drakonaki, EE; Fink, M; Friedrich-Rust, M; Fromageau, J; Havre, RF; Jenssen, C; Ohlinger, R; Săftoiu, A; Schaefer, F; Dietrich, CF; EFSUMB (2013-06)The clinical part of these Guidelines and Recommendations produced under the auspices of the European Federation of Societies for Ultrasound in Medicine and Biology EFSUMB assesses the clinically used applications of all ...
Trial Design and Objectives for Castration-Resistant Prostate Cancer: Updated Recommendations From the Prostate Cancer Clinical Trials Working Group 3. Scher, HI; Morris, MJ; Stadler, WM; Higano, C; Basch, E; Fizazi, K; Antonarakis, ES; Beer, TM; Carducci, MA; Chi, KN; Corn, PG; de Bono, JS; Dreicer, R; George, DJ; Heath, EI; Hussain, M; Kelly, WK; Liu, G; Logothetis, C; Nanus, D; Stein, MN; Rathkopf, DE; Slovin, SF; Ryan, CJ; Sartor, O; Small, EJ; Smith, MR; Sternberg, CN; Taplin, M-E; Wilding, G; Nelson, PS; Schwartz, LH; Halabi, S; Kantoff, PW; Armstrong, AJ; Prostate Cancer Clinical Trials Working Group 3 (2016-04)Purpose Evolving treatments, disease phenotypes, and biology, together with a changing drug development environment, have created the need to revise castration-resistant prostate cancer (CRPC) clinical trial recommendations ...
A genomic approach to therapeutic target validation identifies a glucose-lowering GLP1R variant protective for coronary heart disease. Scott, RA; Freitag, DF; Li, L; Chu, AY; Surendran, P; Young, R; Grarup, N; Stancáková, A; Chen, Y; Varga, TV; Yaghootkar, H; Luan, J; Zhao, JH; Willems, SM; Wessel, J; Wang, S; Maruthur, N; Michailidou, K; Pirie, A; van der Lee, SJ; Gillson, C; Al Olama, AA; Amouyel, P; Arriola, L; Arveiler, D; Aviles-Olmos, I; Balkau, B; Barricarte, A; Barroso, I; Garcia, SB; Bis, JC; Blankenberg, S; Boehnke, M; Boeing, H; Boerwinkle, E; Borecki, IB; Bork-Jensen, J; Bowden, S; Caldas, C; Caslake, M; CVD50 consortium; Cupples, LA; Cruchaga, C; Czajkowski, J; den Hoed, M; Dunn, JA; Earl, HM; Ehret, GB; Ferrannini, E; Ferrieres, J; Foltynie, T; Ford, I; Forouhi, NG; Gianfagna, F; Gonzalez, C; Grioni, S; Hiller, L; Jansson, J-H; Jørgensen, ME; Jukema, JW; Kaaks, R; Kee, F; Kerrison, ND; Key, TJ; Kontto, J; Kote-Jarai, Z; Kraja, AT; Kuulasmaa, K; Kuusisto, J; Linneberg, A; Liu, C; Marenne, G; Mohlke, KL; Morris, AP; Muir, K; Müller-Nurasyid, M; Munroe, PB; Navarro, C; Nielsen, SF; Nilsson, PM; Nordestgaard, BG; Packard, CJ; Palli, D; Panico, S; Peloso, GM; Perola, M; Peters, A; Poole, CJ; Quirós, JR; Rolandsson, O; Sacerdote, C; Salomaa, V; Sánchez, M-J; Sattar, N; Sharp, SJ; Sims, R; Slimani, N; Smith, JA; Thompson, DJ; Trompet, S; Tumino, R; van der A, DL; van der Schouw, YT; Virtamo, J; Walker, M; Walter, K; GERAD_EC Consortium; Neurology Working Group of the Cohorts for Heart; Aging Research in Genomic Epidemiology (CHARGE); Alzheimer’s Disease Genetics Consortium; Pancreatic Cancer Cohort Consortium; European Prospective Investigation into Cancer and Nutrition–Cardiovascular Disease (EPIC-CVD); EPIC-InterAct; Abraham, JE; Amundadottir, LT; Aponte, JL; Butterworth, AS; Dupuis, J; Easton, DF; Eeles, RA; Erdmann, J; Franks, PW; Frayling, TM; Hansen, T; Howson, JMM; Jørgensen, T; Kooner, J; Laakso, M; Langenberg, C; McCarthy, MI; Pankow, JS; Pedersen, O; Riboli, E; Rotter, JI; Saleheen, D; Samani, NJ; Schunkert, H; Vollenweider, P; O'Rahilly, S; CHARGE consortium; CHD Exome+ Consortium; CARDIOGRAM Exome Consortium; Deloukas, P; Danesh, J; Goodarzi, MO; Kathiresan, S; Meigs, JB; Ehm, MG; Wareham, NJ; Waterworth, DM (2016-06)Regulatory authorities have indicated that new drugs to treat type 2 diabetes (T2D) should not be associated with an unacceptable increase in cardiovascular risk. Human genetics may be able to guide development of antidiabetic ...