Who Dies From Prostate Cancer? An Analysis of the Surveillance, Epidemiology and End Results Database

Aims To characterise the presenting features of those who ultimately die from prostate cancer (PCa). Materials and methods The study population consisted of patients in the Surveillance, Epidemiology and End Results (SEER) Program database diagnosed with PCa between 1990 and 2015. Patients were assigned to the following clinical risk groups: low-risk localised (LRL), intermediate-risk localised (IRL), high-risk localised (HRL), node-positive and metastatic (M1). Before 2004, in the absence of prostate-specific antigen (PSA) and Gleason score data, patients with cT1-T2aN0M0 and low-grade PCa were classified as LRL, those with cT3-4N0M0 or high-grade PCa were classified as HRL and all others with N0M0 disease were classified as IRL. The primary aim was to describe the risk group distribution of those who ultimately died from PCa compared with those who were diagnosed with PCa over the study period. A secondary aim was to estimate PCa-specific survival (PCSS) and evaluate the association of risk group with PCSS. Results Among a total of 811 487 patients who were diagnosed with PCa, data sufficient for risk group determination were present in 635 733 patients. The median follow-up was 83 months. The overall risk group distribution at diagnosis was as follows: LRL 10.5%, IRL 49.7%, HRL 34.8%, node-positive 1.5% and M1 3.5%. The risk group distribution of those who died from PCa was 3.9%, 29.4%, 40.9%, 3.2% and 22.8%, respectively. Compared with LRL PCa, the adjusted hazard ratio (95% confidence interval) for PCSS was 1.40 (1.33–1.46) in IRL, 3.76 (3.60–3.93) in HRL, 11.87 (11.14–12.65) in node-positive and 37.12 (35.43–38.88) in M1. Conclusions In this large contemporary cohort, patients with M1, node-positive and HRL disease accounted for two-thirds of all deaths from PCa. De novo metastatic PCa was associated with an approximately 40-fold increased risk of death from PCa compared with LRL PCa. Efforts to improve PCSS will therefore depend largely on improvements in therapy in those with M1, node-positive and HRL disease.