Lauren Folgosa Cooley1, Adaeze A Emeka1, Travis J Meyers2, Phillip R Cooper1, Daniel W Lin3,4, Antonio Finelli5, James A Eastham6, Christopher J Logothetis7, Leonard S Marks8, Danny Vesprini9, S Larry Goldenberg10, Celestia S Higano10, Christian P Pavlovich11, June M Chan2,12, Todd M Morgan13, Eric A Klein14, Daniel A Barocas15, Stacy Loeb16, Brian T Helfand17, Denise M Scholtens18, John S Witte2,12,19, William J Catalona1. 1. Department of Urology, Northwestern University Feinberg School of Medicine, Chicago, Illinois. 2. Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, California. 3. Fred Hutchinson Cancer Research Center, Cancer Prevention Program, Public Health Sciences, Seattle, Washington. 4. Department of Urology, University of Washington, Seattle, Washington. 5. Division of Urology, Department of Surgery, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada. 6. Urology Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York. 7. Departments of Genitourinary Medical Oncology and Urology, the University of Texas M. D. Anderson Cancer Center, Houston, Texas. 8. Department of Urology, David Geffen School of Medicine at UCLA, Los Angeles, California. 9. Odette Cancer Centre, Sunnybrook Health and Sciences Centre, University of Toronto, Toronto, Ontario, Canada. 10. Department of Urologic Sciences, University of British Columbia, Vancouver, British Columbia, Canada. 11. The Brady Urological Institute, the Johns Hopkins University School of Medicine, Baltimore, Maryland. 12. Department of Urology, University of California, San Francisco, San Francisco, California. 13. Department of Urology, University of Michigan, Ann Arbor, Michigan. 14. Glickman Urological and Kidney Institute, Cleveland Clinic Lerner College of Medicine, Cleveland Clinic, Cleveland, Ohio. 15. Department of Urology, Vanderbilt University Medical Center, Nashville, Tennessee. 16. Departments of Urology and Population Health, New York University Langone Health and Manhattan Veterans Affairs Medical Center, New York, New York. 17. Division of Urology, NorthShore University Health System, Evanston, Illinois. 18. Division of Biostatistics, Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois. 19. Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, California.
Abstract
PURPOSE: We examined the demographic and clinicopathological parameters associated with the time to convert from active surveillance to treatment among men with prostate cancer. MATERIALS AND METHODS: A multi-institutional cohort of 7,279 patients managed with active surveillance had data and biospecimens collected for germline genetic analyses. RESULTS: Of 6,775 men included in the analysis, 2,260 (33.4%) converted to treatment at a median followup of 6.7 years. Earlier conversion was associated with higher Gleason grade groups (GG2 vs GG1 adjusted hazard ratio [aHR] 1.57, 95% CI 1.36-1.82; ≥GG3 vs GG1 aHR 1.77, 95% CI 1.29-2.43), serum prostate specific antigen concentrations (aHR per 5 ng/ml increment 1.18, 95% CI 1.11-1.25), tumor stages (cT2 vs cT1 aHR 1.58, 95% CI 1.41-1.77; ≥cT3 vs cT1 aHR 4.36, 95% CI 3.19-5.96) and number of cancerous biopsy cores (3 vs 1-2 cores aHR 1.59, 95% CI 1.37-1.84; ≥4 vs 1-2 cores aHR 3.29, 95% CI 2.94-3.69), and younger age (age continuous per 5-year increase aHR 0.96, 95% CI 0.93-0.99). Patients with high-volume GG1 tumors had a shorter interval to conversion than those with low-volume GG1 tumors and behaved like the higher-risk patients. We found no significant association between the time to conversion and self-reported race or genetic ancestry. CONCLUSIONS: A shorter time to conversion from active surveillance to treatment was associated with higher-risk clinicopathological tumor features. Furthermore, patients with high-volume GG1 tumors behaved similarly to those with intermediate and high-risk tumors. An exploratory analysis of self-reported race and genetic ancestry revealed no association with the time to conversion.
PURPOSE: We examined the demographic and clinicopathological parameters associated with the time to convert from active surveillance to treatment among men with prostate cancer. MATERIALS AND METHODS: A multi-institutional cohort of 7,279 patients managed with active surveillance had data and biospecimens collected for germline genetic analyses. RESULTS: Of 6,775 men included in the analysis, 2,260 (33.4%) converted to treatment at a median followup of 6.7 years. Earlier conversion was associated with higher Gleason grade groups (GG2 vs GG1 adjusted hazard ratio [aHR] 1.57, 95% CI 1.36-1.82; ≥GG3 vs GG1 aHR 1.77, 95% CI 1.29-2.43), serum prostate specific antigen concentrations (aHR per 5 ng/ml increment 1.18, 95% CI 1.11-1.25), tumor stages (cT2 vs cT1 aHR 1.58, 95% CI 1.41-1.77; ≥cT3 vs cT1 aHR 4.36, 95% CI 3.19-5.96) and number of cancerous biopsy cores (3 vs 1-2 cores aHR 1.59, 95% CI 1.37-1.84; ≥4 vs 1-2 cores aHR 3.29, 95% CI 2.94-3.69), and younger age (age continuous per 5-year increase aHR 0.96, 95% CI 0.93-0.99). Patients with high-volume GG1 tumors had a shorter interval to conversion than those with low-volume GG1 tumors and behaved like the higher-risk patients. We found no significant association between the time to conversion and self-reported race or genetic ancestry. CONCLUSIONS: A shorter time to conversion from active surveillance to treatment was associated with higher-risk clinicopathological tumor features. Furthermore, patients with high-volume GG1 tumors behaved similarly to those with intermediate and high-risk tumors. An exploratory analysis of self-reported race and genetic ancestry revealed no association with the time to conversion.
Entities:
Keywords:
human genetics; prostatic neoplasms; race factors; watchful waiting
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