Abstracts from the Mid-Atlantic Section of the AUA 2020

© The Canadian Journal of Urology TM : International Supplement, October 2020 Risk of Harboring Clinically Significant Prostate Cancer after a Negative Fusion Biopsy for PIRADS 4-5 Lesions: a Tertiary Cancer Center Experience A. Higgins 1 ; J. Drevik 1 ; J. Ellis 1 ; B. Ristau 2 ; R. Parsons 3 ; B. Milestone 3 ; L. Levin 3 ; R. Viterbo 3 ; R. Greenberg 3 ; M. Smaldone 3 ; J.Anaokar 3 ; R. Uzzo 3 ;A. Kutikov 3 ; D. Chen 3 1 Einstein Healthcare Network, Philadelphia, PA, USA; 2 University of Connecticut Health, Farmington, CT, USA; 3 Fox Chase Cancer Center, Philadelphia, PA, USA Introduction: Multiparametric MRI (mpMRI) fusion biopsy has revolutionized prostate cancer diagnosis and screening. Little is published on follow-up strategies and outcomes for men who have initial negative fusion biopsies in the setting of PIRADS 4-5 lesions. Herein we describe our experience with this cohort at a tertiary cancer center. Materials & Methods: We reviewed our prospective database of patients who underwent fusion biopsy (n = 804) and identified men with PIRADS 4-5 lesions (73%, n = 585). Of those men, 149 (25%) had a negative initial fusion biopsy. Men who were referred only for biopsy and those lost to follow-up were excluded. We then reviewed follow-up regimens, noting frequency of PSA, mpMRI, and biopsy. Results: Sixty men from July 2014 to March 2019 were included. PSA testing occurred every 6 months in 65% of patients, with another 27% tested yearly. Repeat mpMRI was performed in 32 men (53%) within 1 year, of which 40% were triggered for rising PSA and 60% for screening only. Fifteen repeated biopsy, of which 12 were fusion. Only 1 was found to have clinically significant prostate cancer (Gleason Group 2) on targeted biopsy and underwent prostatectomy.An additional 3 had Gleason Group 1 found on standard 12-core biopsy and remained on active surveillance. The negative predictive value for clinically significant prostate cancer (≥ Gleason Group 2) in men with PIRADS 4-5 lesions with an initially negative fusion biopsy on subsequent workup was 92%. Conclusions: Within our cohort, very fewmen (1.67%) who had high risk mpMRI (PIRADS 4-5) but negative fusion biopsy were then found to have a clinically significant prostate cancer. Longer follow up is needed to understand the risk profile for harboring aggressive disease. Racial Differences in Preoperative Predictors of Pathologic T3a Upstaging in Clinical T1 Renal Cell Carcinoma M. Bruha 1,2,3 ; N. Suss 1 ; T. Monaghan 1 ; V. Flores 1,2,3 ; D. Robins 1,2,3 ; M. Smith 1,2,3 ; L. Hyacinthe 1 ; B. McNeil 1 ; J. Weiss 1 ; A. Weiner 1,2 1 State University of New York - Downstate, Brooklyn, NY, USA; 2 Kings County Hospital Center, Brooklyn, NY, USA; 3 Veterans Affairs NY Harbor Healthcare, Brooklyn, NY, USA Introduction: Some renal cell carcinomas (RCC) appear clinical T1 (cT1) only to be upstaged on final pathology, which affects postoperative management and disease prognosis. Studies to date examining this phenomenon have been conducted with a cohort of mostly Caucasian patients. This study aims to determine rates and preoperative clinical predictive factors of pathologic tumor upstaging among racial minorities with cT1 RCC. Materials & Methods: We queried the National Cancer Data Base to identify patients diagnosedwithAJCC cT1N0M0 RCCwho underwent partial nephrectomy or radical nephrectomy between 2010 and 2015. Patients included in the analysis identified as African-American, Hispanic, Asian Pacific Islander (API) or other minority patient population. Pathologic tumor upstaging was analyzed as T3a- specific upstaging (pT3a). Multivariable logistic regressions were utilized to identify independent predictors of tumor upstaging. Sub-group analyses were performed for each racial group. Results: Overall, there were 19,363 patients analyzed and T3a-specific upstaging was observed in 733 (3.8%) patients. Sub group analysis of upstaged patients observed 314 (3.0%), 290 (4.5%), 87 (4.9%) and 42 (6.0%) for African American, Hispanic, API and other patient groups, respectively. Clinical predictors of pathological T3a (pT3a) upstaging were older age, tumor histology and Fuhrman grades 3-4 for African American patients only. Conclusions: Our study supports the findings of pT3a tumor upstaging in small renal mass RCCwhile also demonstrating inter-racial variability in upstaging rates and preoperative clinical predictors. Furthermore, racial minorities appear to be at lower risk of pathologic tumor upstaging compared to Caucasians, with African Americans at lowest risk. Analysis of Exosome Genomic Results within the PSA Gray Zone (2-10 ng/mL) J. Alter 1 ; R. Tutrone 2 ; M. Donovan 3 ; P. Torkler 1 ; M. Noerholm 1 ; J. Skog 1 1 Exosome Diagnostics, Waltham, MA, USA; 2 Chesapeake Urology Research Associates, Towson, MD, USA; 3 NY Icahn School of Medicine at Mount Sinai, New York, NY, USA Introduction: Over-diagnosis of indolent prostate cancer (PCa), supports the need for non-invasive tools that predict low-grade (Gleason score 6, GS 6) from high- grade (≥ GS 7). We examined the ExoDx™ Prostate (IntelliScore) (EPI) distribution and potential impact on decision-making in men aged 60-70 years old with PSA levels in the gray zone (2-10 ng/mL) as well as artificially binned PSA subgroups within the gray zone in a de-identified dataset from commercial testing. Materials & Methods: First catch urine samples from men presenting for initial or repeat biopsies were submitted to Exosome Diagnostic Laboratory (Waltham, MA, USA). All men were ≥ 50 years with PSAs in the gray zone. Samples were filtered through a 0.8-μm syringe filter and exosomes were isolated and EPI analysis was conducted as previously described. During the period 2016-2019, PSA measurements as well as de-identified EPI scores were available for 2,892 cases. PSAs in the gray zone were segmented into four groups (2-4, 4-6, 6-8 and 8-10 ng/ mL) and EPI distribution was examined in each PSA group. Results: Of the EPI results generated, 2,892 cases had corresponding PSAs and were from men 60-70 years. The EPI score distribution ranged from 0.59 to 99.87 and the PSA distribution ranged from 1.89 to 10.43 (mean 5.80). In the four PSA groups, EPI distribution was remarkably consistent with EPI low risk ranging from 31% to 34% regardless of PSA subgroup. Conclusions: This data demonstrates that Epi risk distribution aligns with prior validation studies and reinforces the lack of association between PSA and EPI risk assignment. Also, in the prior validation studies (N = 1,022), the risk of HGPCa did not appreciably change regardless of binning PSA (2-10 ng/mL) into discrete groups supporting this analysis which demonstrates that patients with PSA in the gray zone appear clinically similar and that EPI analysis provides superior discrimination for high-grade disease pre-biopsy. MP6-03 MP6-02 MP6-01 Poster Session 6: Urologic Oncologic Disease 40