Abstract
Objective: The aim of this study was to create a model for predicting progression-free survival after radical prostatectomy for localized prostate cancer.
Material and methods: The risk of biochemical recurrence (BCR) was modelled in a cohort of 3452 men aged 70 years or younger who were primarily treated with radical prostatectomy after being diagnosed between 2003 and 2006 with localized prostate cancer [clinical stage T1c–T2, Gleason score 5–10, N0/NX, M0/MX, prostate-specific antigen (PSA) < 20 ng/ml]. The cohort was split into two: one cohort for model development (n = 3452) and one for validation (n = 1762). BCR was defined as two increasing PSA values of at least 0.2 ng/ml, initiation of secondary therapy, distant metastases or death from prostate cancer. Multivariable Cox proportional hazard regression was applied, predictive performance was assessed using the bootstrap resampling technique to calculate the c index, and calibration of the model was evaluated by comparing predicted and observed Kaplan–Meier 1 year BCR.
Results: The overall 5 year progression-free survival was 83% after a median follow-up time of 6.8 years in the development cohort and 7.3 years in the validation cohort. The final model included T stage, PSA level, primary and secondary Gleason grade, and number of positive and negative biopsies. The c index for discrimination between high and low risk of recurrence was 0.68. The probability of progression-free survival ranged from 22% to 97% over the range of risk scores in the study population.
Conclusions: This model is based on nationwide population-based data and can be used with a fair predictive accuracy to guide decisions on clinical follow-up after prostatectomy. An online calculator for convenient clinical use of the model is available at www.npcr.se/nomogram
Acknowledgements
This project was made possible by the continuous work of the National Prostate Cancer Register of Sweden (NPCR) steering group: Pär Stattin (chairman), Anders Widmark, Camilla Thellenberg, Ove Andrén, Anna Bill-Axelson, Ann-Sofi Fransson, Magnus Törnblom, Stefan Carlsson, Marie Hjälm-Eriksson, Bill Pettersson, David Robinson, Mats Andén, Jan-Erik Damber, Jonas Hugosson, Ingela Franck Lissbrant, Maria Nyberg, Göran Ahlgren, Ola Bratt, René Blom, Lars Egevad, Calle Walller, Olof Akre, Per Fransson, Eva Johansson, Fredrik Sandin, Hans Garmo, Mats Lambe and Karin Hellström.
Disclosure statement
No potential conflict of interest was reported by the authors.
Funding information
Financial support came from the Swedish Research Council [K2014-66X-20760-07-4] to AB and [825-2012-5047] to PS, the Swedish Cancer Society [14 0274] to AB, [13 0428] to PS, [2011 825] to OA, and [12 0475] to OB, Governmental funding through Lund University (ALF) to AB, the local cancer foundation at Skåne University Hospital Malmö and the Gunnar Nilsson Cancer Foundation, and a grant from IPSEN, Sweden to AB.