Predicting biochemical recurrence and prostate cancer‐specific mortality after radical prostatectomy: comparison of six prediction models in a cohort of patients with screening‐ and clinically detected prostate cancer

Objectives To perform a comparison and external validation of three models predicting biochemical recurrence (BCR) and three models predicting prostate cancer (PCa)‐specific mortality (PCSM) in a screening setting, i.e. patients with screening‐detected PCa (S‐PCa) and in those with clinically detect...

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Published inBJU international Vol. 124; no. 4; pp. 635 - 642
Main Authors Remmers, Sebastiaan, Verbeek, Jan F. M., Nieboer, Daan, Kwast, Theo, Roobol, Monique J.
Format Journal Article
LanguageEnglish
Published England Wiley Subscription Services, Inc 01.10.2019
John Wiley and Sons Inc
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Abstract Objectives To perform a comparison and external validation of three models predicting biochemical recurrence (BCR) and three models predicting prostate cancer (PCa)‐specific mortality (PCSM) in a screening setting, i.e. patients with screening‐detected PCa (S‐PCa) and in those with clinically detected PCa (C‐PCa). Subjects and Methods We retrospectively evaluated 795 men with S‐PCa, from the European Randomized Study of Screening for Prostate Cancer, Rotterdam, and 1123 men with C‐PCa initially treated with RP. The discriminative ability of the models was assessed according to the area under the curve (AUC) of the receiver‐operating characteristic, and calibration was assessed graphically using calibration plots. Results The median (interquartile range [IQR]) follow‐up for the S‐PCa group was 10.4 (6.8–14.3) years and for the C‐PCa group it was 8.8 (4.8–12.9) years. A total of 123 men with S‐PCa (15%) and 389 men with C‐PCa (35%) experienced BCR. Of the men with S‐PCa and BCR, 24 (20%) died from PCa and 29 (23%) died from other causes. Of the men with C‐PCa and BCR, 68 (17%) died from PCa and 105 (27%) died from other causes. The discrimination of the models predicting BCR or PCSM was higher for men with S‐PCa (AUC: BCR 0.77–0.84, PCSM 0.60–0.77) than for the men with C‐PCa (AUC: BCR 0.75–0.79, PCSM 0.51–0.68) as a result of the similar patient characteristics of the men with S‐PCa in the present study and those of the cohorts used to develop these models. The risk of BCR was typically overestimated, while the risk of PCSM was typically underestimated. Conclusion Prediction models for BCR showed good discrimination and reasonable calibration for both men with S‐PCa and men with C‐PCa, and even better discrimination for men with S‐PCa. For PCSM, the evaluated models are not applicable in both settings of this Dutch cohort as a result of substantial miscalibration. This warrants caution when using these models to communicate future risks in other clinical settings.
AbstractList To perform a comparison and external validation of three models predicting biochemical recurrence (BCR) and three models predicting prostate cancer (PCa)-specific mortality (PCSM) in a screening setting, i.e. patients with screening-detected PCa (S-PCa) and in those with clinically detected PCa (C-PCa). We retrospectively evaluated 795 men with S-PCa, from the European Randomized Study of Screening for Prostate Cancer, Rotterdam, and 1123 men with C-PCa initially treated with RP. The discriminative ability of the models was assessed according to the area under the curve (AUC) of the receiver-operating characteristic, and calibration was assessed graphically using calibration plots. The median (interquartile range [IQR]) follow-up for the S-PCa group was 10.4 (6.8-14.3) years and for the C-PCa group it was 8.8 (4.8-12.9) years. A total of 123 men with S-PCa (15%) and 389 men with C-PCa (35%) experienced BCR. Of the men with S-PCa and BCR, 24 (20%) died from PCa and 29 (23%) died from other causes. Of the men with C-PCa and BCR, 68 (17%) died from PCa and 105 (27%) died from other causes. The discrimination of the models predicting BCR or PCSM was higher for men with S-PCa (AUC: BCR 0.77-0.84, PCSM 0.60-0.77) than for the men with C-PCa (AUC: BCR 0.75-0.79, PCSM 0.51-0.68) as a result of the similar patient characteristics of the men with S-PCa in the present study and those of the cohorts used to develop these models. The risk of BCR was typically overestimated, while the risk of PCSM was typically underestimated. Prediction models for BCR showed good discrimination and reasonable calibration for both men with S-PCa and men with C-PCa, and even better discrimination for men with S-PCa. For PCSM, the evaluated models are not applicable in both settings of this Dutch cohort as a result of substantial miscalibration. This warrants caution when using these models to communicate future risks in other clinical settings.
ObjectivesTo perform a comparison and external validation of three models predicting biochemical recurrence (BCR) and three models predicting prostate cancer (PCa)‐specific mortality (PCSM) in a screening setting, i.e. patients with screening‐detected PCa (S‐PCa) and in those with clinically detected PCa (C‐PCa).Subjects and MethodsWe retrospectively evaluated 795 men with S‐PCa, from the European Randomized Study of Screening for Prostate Cancer, Rotterdam, and 1123 men with C‐PCa initially treated with RP. The discriminative ability of the models was assessed according to the area under the curve (AUC) of the receiver‐operating characteristic, and calibration was assessed graphically using calibration plots.ResultsThe median (interquartile range [IQR]) follow‐up for the S‐PCa group was 10.4 (6.8–14.3) years and for the C‐PCa group it was 8.8 (4.8–12.9) years. A total of 123 men with S‐PCa (15%) and 389 men with C‐PCa (35%) experienced BCR. Of the men with S‐PCa and BCR, 24 (20%) died from PCa and 29 (23%) died from other causes. Of the men with C‐PCa and BCR, 68 (17%) died from PCa and 105 (27%) died from other causes. The discrimination of the models predicting BCR or PCSM was higher for men with S‐PCa (AUC: BCR 0.77–0.84, PCSM 0.60–0.77) than for the men with C‐PCa (AUC: BCR 0.75–0.79, PCSM 0.51–0.68) as a result of the similar patient characteristics of the men with S‐PCa in the present study and those of the cohorts used to develop these models. The risk of BCR was typically overestimated, while the risk of PCSM was typically underestimated.ConclusionPrediction models for BCR showed good discrimination and reasonable calibration for both men with S‐PCa and men with C‐PCa, and even better discrimination for men with S‐PCa. For PCSM, the evaluated models are not applicable in both settings of this Dutch cohort as a result of substantial miscalibration. This warrants caution when using these models to communicate future risks in other clinical settings.
To perform a comparison and external validation of three models predicting biochemical recurrence (BCR) and three models predicting prostate cancer (PCa)-specific mortality (PCSM) in a screening setting, i.e. patients with screening-detected PCa (S-PCa) and in those with clinically detected PCa (C-PCa).OBJECTIVESTo perform a comparison and external validation of three models predicting biochemical recurrence (BCR) and three models predicting prostate cancer (PCa)-specific mortality (PCSM) in a screening setting, i.e. patients with screening-detected PCa (S-PCa) and in those with clinically detected PCa (C-PCa).We retrospectively evaluated 795 men with S-PCa, from the European Randomized Study of Screening for Prostate Cancer, Rotterdam, and 1123 men with C-PCa initially treated with RP. The discriminative ability of the models was assessed according to the area under the curve (AUC) of the receiver-operating characteristic, and calibration was assessed graphically using calibration plots.SUBJECTS AND METHODSWe retrospectively evaluated 795 men with S-PCa, from the European Randomized Study of Screening for Prostate Cancer, Rotterdam, and 1123 men with C-PCa initially treated with RP. The discriminative ability of the models was assessed according to the area under the curve (AUC) of the receiver-operating characteristic, and calibration was assessed graphically using calibration plots.The median (interquartile range [IQR]) follow-up for the S-PCa group was 10.4 (6.8-14.3) years and for the C-PCa group it was 8.8 (4.8-12.9) years. A total of 123 men with S-PCa (15%) and 389 men with C-PCa (35%) experienced BCR. Of the men with S-PCa and BCR, 24 (20%) died from PCa and 29 (23%) died from other causes. Of the men with C-PCa and BCR, 68 (17%) died from PCa and 105 (27%) died from other causes. The discrimination of the models predicting BCR or PCSM was higher for men with S-PCa (AUC: BCR 0.77-0.84, PCSM 0.60-0.77) than for the men with C-PCa (AUC: BCR 0.75-0.79, PCSM 0.51-0.68) as a result of the similar patient characteristics of the men with S-PCa in the present study and those of the cohorts used to develop these models. The risk of BCR was typically overestimated, while the risk of PCSM was typically underestimated.RESULTSThe median (interquartile range [IQR]) follow-up for the S-PCa group was 10.4 (6.8-14.3) years and for the C-PCa group it was 8.8 (4.8-12.9) years. A total of 123 men with S-PCa (15%) and 389 men with C-PCa (35%) experienced BCR. Of the men with S-PCa and BCR, 24 (20%) died from PCa and 29 (23%) died from other causes. Of the men with C-PCa and BCR, 68 (17%) died from PCa and 105 (27%) died from other causes. The discrimination of the models predicting BCR or PCSM was higher for men with S-PCa (AUC: BCR 0.77-0.84, PCSM 0.60-0.77) than for the men with C-PCa (AUC: BCR 0.75-0.79, PCSM 0.51-0.68) as a result of the similar patient characteristics of the men with S-PCa in the present study and those of the cohorts used to develop these models. The risk of BCR was typically overestimated, while the risk of PCSM was typically underestimated.Prediction models for BCR showed good discrimination and reasonable calibration for both men with S-PCa and men with C-PCa, and even better discrimination for men with S-PCa. For PCSM, the evaluated models are not applicable in both settings of this Dutch cohort as a result of substantial miscalibration. This warrants caution when using these models to communicate future risks in other clinical settings.CONCLUSIONPrediction models for BCR showed good discrimination and reasonable calibration for both men with S-PCa and men with C-PCa, and even better discrimination for men with S-PCa. For PCSM, the evaluated models are not applicable in both settings of this Dutch cohort as a result of substantial miscalibration. This warrants caution when using these models to communicate future risks in other clinical settings.
Objectives To perform a comparison and external validation of three models predicting biochemical recurrence (BCR) and three models predicting prostate cancer (PCa)‐specific mortality (PCSM) in a screening setting, i.e. patients with screening‐detected PCa (S‐PCa) and in those with clinically detected PCa (C‐PCa). Subjects and Methods We retrospectively evaluated 795 men with S‐PCa, from the European Randomized Study of Screening for Prostate Cancer, Rotterdam, and 1123 men with C‐PCa initially treated with RP. The discriminative ability of the models was assessed according to the area under the curve (AUC) of the receiver‐operating characteristic, and calibration was assessed graphically using calibration plots. Results The median (interquartile range [IQR]) follow‐up for the S‐PCa group was 10.4 (6.8–14.3) years and for the C‐PCa group it was 8.8 (4.8–12.9) years. A total of 123 men with S‐PCa (15%) and 389 men with C‐PCa (35%) experienced BCR. Of the men with S‐PCa and BCR, 24 (20%) died from PCa and 29 (23%) died from other causes. Of the men with C‐PCa and BCR, 68 (17%) died from PCa and 105 (27%) died from other causes. The discrimination of the models predicting BCR or PCSM was higher for men with S‐PCa (AUC: BCR 0.77–0.84, PCSM 0.60–0.77) than for the men with C‐PCa (AUC: BCR 0.75–0.79, PCSM 0.51–0.68) as a result of the similar patient characteristics of the men with S‐PCa in the present study and those of the cohorts used to develop these models. The risk of BCR was typically overestimated, while the risk of PCSM was typically underestimated. Conclusion Prediction models for BCR showed good discrimination and reasonable calibration for both men with S‐PCa and men with C‐PCa, and even better discrimination for men with S‐PCa. For PCSM, the evaluated models are not applicable in both settings of this Dutch cohort as a result of substantial miscalibration. This warrants caution when using these models to communicate future risks in other clinical settings.
Author Nieboer, Daan
Kwast, Theo
Verbeek, Jan F. M.
Roobol, Monique J.
Remmers, Sebastiaan
AuthorAffiliation 2 Department of Public Health Erasmus University Medical Centre Rotterdam The Netherlands
4 Department of Pathology Toronto General Hospital Toronto ON Canada
1 Department of Urology Erasmus University Medical Centre Rotterdam The Netherlands
3 Department of Pathology Erasmus University Medical Centre Rotterdam The Netherlands
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Issue 4
Keywords nomograms
probability
prostatic neoplasms
PCSM
ProstateCancer
prostatectomy
clinical decision-making
Language English
License Attribution-NonCommercial-NoDerivs
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31901011 - BJU Int. 2020 Jan;125(1):190. doi: 10.1111/bju.14949
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Snippet Objectives To perform a comparison and external validation of three models predicting biochemical recurrence (BCR) and three models predicting prostate cancer...
To perform a comparison and external validation of three models predicting biochemical recurrence (BCR) and three models predicting prostate cancer...
ObjectivesTo perform a comparison and external validation of three models predicting biochemical recurrence (BCR) and three models predicting prostate cancer...
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SubjectTerms Calibration
Cancer surgery
Clinical decision making
Mortality
nomograms
PCSM
Prediction models
probability
Prostate cancer
ProstateCancer
Prostatectomy
prostatic neoplasms
Urological Oncology
Urological surgery
Title Predicting biochemical recurrence and prostate cancer‐specific mortality after radical prostatectomy: comparison of six prediction models in a cohort of patients with screening‐ and clinically detected prostate cancer
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fbju.14790
https://www.ncbi.nlm.nih.gov/pubmed/31055875
https://www.proquest.com/docview/2293781371
https://www.proquest.com/docview/2232110508
https://pubmed.ncbi.nlm.nih.gov/PMC6852479
Volume 124
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