PROPOSE: Active surveillance has been endorsed for low-risk prostate cancer, but information about long-term outcomes and comparative effectiveness of active surveillance is lacking.
The purpose of this study is to project prostate cancer mortality under active surveillance followed by radical prostatectomy versus under immediate radical prostatectomy.
EXPERIMENTAL DESIGN: A simulation model was developed to combine information on time from diagnosis to treatment under active surveillance and associated disease progression from a Johns Hopkins active surveillance cohort (n = 769), time from radical prostatectomy to recurrence from cases in the CaPSURE database with T-stage ≤ T2a (n = 3,470), and time from recurrence to prostate cancer death from a T-stage ≤ T2a Johns Hopkins cohort of patients whose disease recurred after radical prostatectomy (n = 963). Results were projected for a hypothetical cohort aged 40 to 90 years with low-risk prostate cancer (T-stage ≤ T2a, Gleason score ≤ 6, and prostate-specific antigen level ≤ 10 ng/mL).
RESULTS: The model projected that 2.8% of men on active surveillance and 1.6% of men with immediate radical prostatectomy would die of their disease in 20 years. Corresponding lifetime estimates were 3.4% for active surveillance and 2.0% for immediate radical prostatectomy. The average projected increase in life expectancy associated with immediate radical prostatectomy was 1.8 months. On average, the model projected that men on active surveillance would remain free of treatment for an additional 6.4 years relative to men treated immediately.
CONCLUSIONS: Active surveillance is likely to produce a very modest decline in prostate cancer-specific survival among men diagnosed with low-risk prostate cancer but could lead to significant benefits in terms of quality of life.
Written by:
Xia J, Trock BJ, Cooperberg MR, Gulati R, Zeliadt SB, Gore JL, Lin DW, Carroll PR, Carter HB, Etzioni R. Are you the author?
Division of Public Health Sciences, Fred Hutchinson Cancer Research Center; VA Health Services Research & Development; Department of Urology, University of Washington, Seattle, Washington; Departments of Urology, Epidemiology, Oncology, and Environmental Health Sciences; James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland; and Department of Urology, UCSF Helen Diller Family Comprehensive Cancer Center, San Francisco, California.
Reference: Clin Cancer Res. 2012 Oct 1;18(19):5471-5478.
doi: 10.1158/1078-0432.CCR-12-1502
PubMed Abstract
PMID: 23008476
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