John A Brockman1, Shaheen Alanee2, Andrew J Vickers3, Peter T Scardino2, David P Wood4, Adam S Kibel5, Daniel W Lin6, Fernando J Bianco7, Danny M Rabah8, Eric A Klein9, Jay P Ciezki10, Tianming Gao11, Michael W Kattan11, Andrew J Stephenson12. 1. Glickman Urological and Kidney Institute, Cleveland Clinic, Cleveland, OH, USA; Case Western Reserve University School of Medicine, Cleveland, OH, USA. 2. Division of Urology, Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. 3. Division of Urology, Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, NY, USA; Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. 4. Department of Urology, University of Michigan, Ann Arbor, MI, USA. 5. Division of Urologic Surgery, Washington University School of Medicine, St. Louis, MO, USA. 6. Department of Urology, University of Washington School of Medicine, Seattle, WA, USA. 7. Department of Urology, Columbia University, New York, NY, USA. 8. Division of Urology, Department of Surgery, Princess Johara Alibrahim Center for Cancer Research, King Saud University, Riyadh, Saudi Arabia. 9. Glickman Urological and Kidney Institute, Cleveland Clinic, Cleveland, OH, USA; Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA. 10. Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA. 11. Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH, USA. 12. Glickman Urological and Kidney Institute, Cleveland Clinic, Cleveland, OH, USA; Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: stephena2@ccf.org.
Abstract
BACKGROUND: The natural history of prostate-specific antigen (PSA)-defined biochemical recurrence (BCR) of prostate cancer (PCa) after definitive local therapy is highly variable. Validated prediction models for PCa-specific mortality (PCSM) in this population are needed for treatment decision-making and clinical trial design. OBJECTIVE: To develop and validate a nomogram to predict the probability of PCSM from the time of BCR among men with rising PSA levels after radical prostatectomy. DESIGN, SETTING, AND PARTICIPANTS: Between 1987 and 2011, 2254 men treated by radical prostatectomy at one of five high-volume hospitals experienced BCR, defined as three successive PSA rises (final value >0.2 ng/ml), single PSA >0.4 ng/ml, or use of secondary therapy administered for detectable PSA >0.1 ng/ml. Clinical information and follow-up data were modeled using competing-risk regression analysis to predict PCSM from the time of BCR. INTERVENTION: Radical prostatectomy for localized prostate cancer and subsequent PCa BCR. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: PCSM. RESULTS AND LIMITATIONS: The 10-yr PCSM and mortality from competing causes was 19% (95% confidence interval [CI] 16-21%) and 17% (95% CI 14-19%), respectively. A nomogram predicting PCSM for all patients had an internally validated concordance index of 0.774. Inclusion of PSA doubling time (PSADT) in a nomogram based on standard parameters modestly improved predictive accuracy (concordance index 0.763 vs 0.754). Significant parameters in the models were preoperative PSA, pathological Gleason score, extraprostatic extension, seminal vesicle invasion, time to PCa BCR, PSA level at PCa BCR, and PSADT (all p<0.05). CONCLUSIONS: We constructed and validated a nomogram to predict the risk of PCSM at 10 yr among men with PCa BCR after radical prostatectomy. The nomogram may be used for patient counseling and the design of clinical trials for PCa. PATIENT SUMMARY: For men with biochemical recurrence of prostate cancer after radical prostatectomy, we have developed a model to predict the long-term risk of death from prostate cancer.
BACKGROUND: The natural history of prostate-specific antigen (PSA)-defined biochemical recurrence (BCR) of prostate cancer (PCa) after definitive local therapy is highly variable. Validated prediction models for PCa-specific mortality (PCSM) in this population are needed for treatment decision-making and clinical trial design. OBJECTIVE: To develop and validate a nomogram to predict the probability of PCSM from the time of BCR among men with rising PSA levels after radical prostatectomy. DESIGN, SETTING, AND PARTICIPANTS: Between 1987 and 2011, 2254 men treated by radical prostatectomy at one of five high-volume hospitals experienced BCR, defined as three successive PSA rises (final value >0.2 ng/ml), single PSA >0.4 ng/ml, or use of secondary therapy administered for detectable PSA >0.1 ng/ml. Clinical information and follow-up data were modeled using competing-risk regression analysis to predict PCSM from the time of BCR. INTERVENTION: Radical prostatectomy for localized prostate cancer and subsequent PCa BCR. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: PCSM. RESULTS AND LIMITATIONS: The 10-yr PCSM and mortality from competing causes was 19% (95% confidence interval [CI] 16-21%) and 17% (95% CI 14-19%), respectively. A nomogram predicting PCSM for all patients had an internally validated concordance index of 0.774. Inclusion of PSA doubling time (PSADT) in a nomogram based on standard parameters modestly improved predictive accuracy (concordance index 0.763 vs 0.754). Significant parameters in the models were preoperative PSA, pathological Gleason score, extraprostatic extension, seminal vesicle invasion, time to PCa BCR, PSA level at PCa BCR, and PSADT (all p<0.05). CONCLUSIONS: We constructed and validated a nomogram to predict the risk of PCSM at 10 yr among men with PCa BCR after radical prostatectomy. The nomogram may be used for patient counseling and the design of clinical trials for PCa. PATIENT SUMMARY: For men with biochemical recurrence of prostate cancer after radical prostatectomy, we have developed a model to predict the long-term risk of death from prostate cancer.
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