Impact of percent positive biopsy cores on cancer-specific mortality for patients with high-risk prostate cancer.

2018 ◽  
Vol 36 (6_suppl) ◽  
pp. 78-78
Author(s):  
David Dewei Yang ◽  
Vinayak Muralidhar ◽  
Brandon Arvin Virgil Mahal ◽  
Marie Vastola ◽  
Ninjiin Boldbaatar ◽  
...  

78 Background: A high percent positive biopsy cores (PBC), typically dichotomized at ≥50%, is prognostic of worse cancer-specific outcomes for patients with low- and intermediate-risk prostate cancer. The prognostic value of ≥50% PBC for patients with high-risk disease is poorly understood. We examined the association between ≥50% PBC and prostate cancer-specific mortality (PCSM) for patients with high-risk prostate cancer. Methods: We identified 7,569 men from the Surveillance, Epidemiology, and End Results program who were diagnosed with high-risk prostate cancer (Gleason 8-10, prostate-specific antigen > 20 ng/mL, or cT3-T4 stage without evidence of nodal or metastatic disease) in 2010 or 2011 and had 6-24 cores sampled at biopsy. Multivariable Fine and Gray competing risks regression was utilized to examine the association between ≥50% PBC and PCSM, with adjustments for sociodemographic and clinicopathologic factors. Results: Median follow-up was 3.8 years (interquartile range 3.3-4.3 years). 56.2% of patients (4,253) had ≥50% PBC. The 4-year unadjusted cumulative incidences of PCSM were 2.0% (95% confidence interval [CI] 1.5-2.6%) and 5.6% (95% CI 4.9-6.4%) for patients with < 50% and ≥50% PBC, respectively. On multivariable analysis, the presence of ≥50% PBC was associated with a significantly higher risk of PCSM (adjusted hazard ratio [AHR] 1.95, 95% CI 1.43-2.66, P< 0.001). On subgroup analysis, ≥50% PBC was associated with a significantly higher risk of PCSM only for cT1-T2 disease (AHR 2.21, 95% CI 1.59-3.07, P< 0.001) but not cT3-T4 disease (AHR 0.77, 95% CI 0.33-1.81, P= 0.547), with a significant interaction ( Pinteraction= 0.012). Conclusions: In this large, contemporary cohort of patients with high-risk prostate cancer, ≥50% PBC was independently associated with a two-fold increased risk of PCSM for patients with cT1-T2, but not cT3-T4, tumors. Percent PBC should be used to routinely risk stratify men with high-risk disease and identify patients who may benefit from intensification of therapy, such as adding docetaxel or abiraterone to radiotherapy with androgen deprivation therapy, to optimize cancer-specific outcomes.

2020 ◽  
Vol 38 (9) ◽  
pp. 735.e9-735.e15
Author(s):  
David D. Yang ◽  
Vinayak Muralidhar ◽  
Brandon A. Mahal ◽  
Marie E. Vastola ◽  
Ninjin Boldbaatar ◽  
...  

2016 ◽  
Vol 34 (2_suppl) ◽  
pp. 52-52
Author(s):  
Vinayak Muralidhar ◽  
MIchael H. Xiang ◽  
Peter F. Orio ◽  
Neil E. Martin ◽  
Clair Beard ◽  
...  

52 Background: A randomized trial has recently reported improved 5-year biochemical recurrence-free survival with brachytherapy (BT) boost compared with external beam radiation therapy (EBRT) boost in intermediate- to high-risk prostate cancer. Recent retrospective data suggest that BT boost may also confer a cancer-specific survival benefit in the high-risk subgroup. We sought to determine whether this survival benefit would extend to the recently defined favorable high-risk subgroup of prostate cancer patients (T1c, Gleason 4+4 = 8, PSA < 10 ng/mL or T1c, Gleason 6, PSA > 20 ng/mL). Methods: We identified 45,078 patients in the Surveillance, Epidemiology, and End Results database with cT1c-T3aN0M0 intermediate- to high-risk prostate cancer diagnosed 2004-2011 treated with EBRT or EBRT plus BT. We used multivariable competing risks regression to determine differences in the rate of prostate cancer-specific mortality (PCSM) after EBRT+BT or EBRT alone in patients with intermediate-risk, favorable high-risk, or other high-risk disease after adjusting for demographic and clinical factors. Results: BT boost was not associated with an improvement in 5-year PCSM compared with EBRT alone among patients with favorable high-risk disease (1.6% vs 1.9%; adjusted hazard ratio [AHR] 0.56; 95% confidence interval [CI], 0.21 to 1.52, P = 0.258) and intermediate-risk disease (0.7% vs 0.9%; AHR 0.83; 95% CI, 0.59 to 1.16; P = 0.270). Others with high-risk disease had significantly lower 5-year PCSM when treated with BT boost compared with EBRT alone (3.9% vs 5.0%; AHR 0.73; 95% CI, 0.55 to 0.95; P = 0.022). Conclusions: Brachytherapy boost is associated with a decreased rate of PCSM in men with high-risk prostate cancer, but this benefit was not seen among patients with favorable high-risk disease. This suggests that the recently-defined “favorable high-risk” category may be used to personalize therapy for men with high risk disease.


Cancer ◽  
2010 ◽  
Vol 116 (11) ◽  
pp. 2590-2595 ◽  
Author(s):  
Karen E. Hoffman ◽  
Ming-Hui Chen ◽  
Brian J. Moran ◽  
Michelle H. Braccioforte ◽  
Daniel Dosoretz ◽  
...  

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e16004-e16004 ◽  
Author(s):  
Rahul D. Tendulkar ◽  
Michael W. Kattan ◽  
Changhong Yu ◽  
Chandana A. Reddy ◽  
Kevin L. Stephans ◽  
...  

e16004 Background: Men receiving high dose external beam radiotherapy (EBRT) and androgen deprivation therapy (ADT) for high risk prostate cancer (HRPC) have other competing causes of mortality, however predictive schema do not account for patient-related co-morbidities. We aim to create nomograms estimating all-cause mortality (ACM) and prostate cancer-specific mortality (PCSM) in this population. Methods: 660 patients with HRPC defined by NCCN guidelines were treated with EBRT ≥74 Gy and ADT from 1996-2009. The probabilities of death from prostate cancer and other causes were estimated by cumulative incidence function. Multivariable Cox proportional hazards regression and competing risks regression analyses were used for modeling ACM and PCSM respectively. Deaths from other causes were treated as competing risks for PCSM. Missing values in the predictors were multiply imputed before conducting multivariable regression analysis. Variables investigated were age, clinical T stage, prostate specific antigen (PSA), Gleason score, race, family history, duration of ADT, body mass index (BMI), Charlson co-morbidity index score, coronary artery disease, and smoking pack-years. The stepdown method was used to make parsimonious models based on the rank of the predictive ability of each variable with respect to each endpoint. The final nomograms were internally validated by assessing the discrimination and calibration with bootstrap resamples. Results: At last follow up, there were 199 deaths. The 10-year cumulative incidence of death from prostate cancer was 14% and from other causes was 26%. The variables that predicted for 10-year ACM included age, PSA, BMI, Charlson score, and smoking pack-years. The ACM nomogram achieved a concordance index of 0.672. The variables that predicted for PCSM included Gleason score, PSA, race, and duration of ADT. The nomogram concordance index for PCSM was 0.673. The calibrations for both ACM and PCSM appear reasonable. Conclusions: We have developed nomograms that predict for ACM and PCSM in men with aggressive prostate cancer and competing risks of death. External validation may be useful.


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