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PD59-02 VARIABILITY IN GROWTH KINETICS OF SMALL RENAL MASSES ON ACTIVE SURVEILLANCE: RESULTS FROM THE DISSRM REGISTRY
THE JOURNAL OF UROLOGYâ
Vol. 197, No. 4S, Supplement, Monday, May 15, 2017
free survival. Progression was strictly defined as growth rate >0.5 cm/year, greatest tumor diameter >4.0 cm, metastatic disease, or elective crossover. Outcomes were evaluated using Kaplan-Meier survival analysis and comparisons were performed using the log-rank test. RESULTS: Of the 615 enrolled patients, 298 (48.5%) chose primary intervention and 317 (51.5%) chose active surveillance. From the active surveillance cohort, 45 (14.2%) patients underwent delayed intervention. Median follow-up time for the entire registry was 2.9 years, with 203 (33.0%) patients followed for 5 years or more. At baseline, patients who chose active surveillance were older (P < 0.001) and had higher comorbidity status (P < 0.001) than those who chose primary intervention. There was no difference in cancer-specific survival at 7 years between primary intervention and active surveillance (99.0% vs 100%, respectively, P ¼ 0.3) [Figure 1A]. However, overall survival was higher in patients with primary intervention when compared to active surveillance at 5 years (93.0% vs 80.2%, respectively) and 7 years (91.7% vs 65.9%, respectively, P ¼ 0.002) [Figure 1B]. The 5-year and 7-year progression-free survival rate in the active surveillance cohort was 83.9% and 71.4%, respectively. CONCLUSIONS: In the intermediate-term, active surveillance appears to be as safe as and not inferior to primary intervention for carefully selected patients with small renal masses. As the registry matures, further studies will elucidate the effectiveness of active surveillance in the long-term.
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trigger reflex crossover to intervention as growth rates are highly variable within the first 6-12 months of surveillance. Instead we recommend re-assessment of risk stratification with additional imaging or consideration of biopsy prior to treatment. The role of GR in decision making for SRM on AS requires further refinement.
Source of Funding: Research reported in this abstract was supported by the TL1 Predoctoral Training Program of the National Institutes of Health under award number TL1200008. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Source of Funding: National Institutes of Health (NIH), Grant Number TL1 TR001078.
PD59-02 VARIABILITY IN GROWTH KINETICS OF SMALL RENAL MASSES ON ACTIVE SURVEILLANCE: RESULTS FROM THE DISSRM REGISTRY Akachimere Uzosike*, Michael Johnson, Hiten Patel, Mark Riffon, Michael Gorin, Christian Pavlovich, Baltimore, MD; Peter Chang, Andrew Wagner, Boston, MA; Bruce Trock, Mohamad Allaf, Phillip Pierorazio, Baltimore, MD INTRODUCTION AND OBJECTIVES: Active surveillance (AS) is emerging as a safe and effective strategy for the management of small renal masses, which are defined as solid masses with a maximum diameter less than 4.0cm. We conducted this prospective multi-institutional study involving patients with small renal masses in order to characterize the growth rates of these masses and their pertinence to clinical outcomes. METHODS: Beginning in 2009, the Delayed Intervention and Surveillance for Small Renal Masses (DISSRM), a prospective multiinstitutional registry of patients with small renal masses, has enrolled patients who chose either primary intervention or AS. Patients electing active surveillance received regularly scheduled imaging, with tumor characteristics collected throughout their enrollment in the registry. RESULTS: 615 patients were prospectively enrolled, of which 317 patients (51.5%) elected AS. 284 had follow-up imaging at time of this analysis, with a mean follow-up of 2.91 years. Overall mean growth rate was -0.11 cm0.31cm/year (median: -0.07 cm/year). Growth rate and variability decreased with time, with the mean growth rates at 6, 12, 24, and 48 months of -0.100.09, -0.08 0.07, -0.050.056, and -0.040.02 cm/ year, respectively (Figure 1). GR was not predictive of adverse pathological features. No patient developed metastatic disease or died of kidney cancer. CONCLUSIONS: Growth kinetics of SRM is highly variable upon entrance into AS, with both growth rate and growth rate variability decreasing with time. Early in AS, worrisome growth rates should not
PD59-03 GROWTH KINETICS IN VON HIPPEL-LINDAU-ASSOCIATED RENAL TUMORS: DEFINING THE INFLUENCE OF GERMLINE MUTATION TYPE Mark Ball*, Shawna Boyle, Bethesda, MD; Kiranpreet Khurana, Cleveland, OH; Rabindra Gautam, Bethesda, MD; Gennady Bratslavsky, Syracuse, NY; W. Marston Linehan, Adam Metwalli, Bethesda, MD INTRODUCTION AND OBJECTIVES: Renal cell carcinoma develops in 25-60% of patients von Hippel-Lindau (VHL), which is characterized by germline mutations in the VHL gene. The paradigm for treating renal tumors in VHL includes active surveillance for lesions less than 3 cm, and surgical resection for lesions greater than 3 cm. Knowledge of growth rates for renal lesions in VHL guide surveillance schedules. While the risk of developing RCC is related to VHL genotype, it is unknown if VHL genotype can influence tumor growth rate. We sought to characterize growth rate for VHL-associated renal tumors and to determine if the type of germline mutation in VHL influences tumor growth kinetics. METHODS: Patients with solid, enhancing renal tumors with at least 3 cross sectional imaging studies and known germline mutation status were retrospectively reviewed. In patients with multiple index lesions, all lesions were analyzed. Renal tumor size was measured as the largest single-dimension diameter. Growth rates were calculated using linear regression. Germline mutations were categorized into missense, partial deletion, frameshift, deletion, splice donor, amino acid insertion, and splice acceptor. The effect of germline mutation type on renal tumor kinetics was assessed with the Wilcoxon-ranksum or Kruskall Wallis tests. RESULTS: A total of 246 tumors in 161 patients and 1341 timepoint measurements were included for analysis. Median growth rate for the entire cohort was 3.5 mm (interquartile range 2.4-5.1 mm). Median growth rates were similar for all mutation categories: 3.4 mm for missense (n¼111), 3.5 mm for partial deletion (n¼71), 3.2 mm for nonsense (n¼28), 4.5 mm for frameshift (n¼16), 2.5 mm for deletion (n¼8), 3.4 mm for splice donor (n¼4), 3.9 mm for amino acid insertion (n¼3), and 4.9 mm for splice acceptor (n¼3) (Figure 1). There was no difference in growth rates between missense and non-missense tumors (p¼0.1)
Vol. 197, No. 4S, Supplement, Monday, May 15, 2017
free survival. Progression was strictly defined as growth rate >0.5 cm/year, greatest tumor diameter >4.0 cm, metastatic disease, or elective crossover. Outcomes were evaluated using Kaplan-Meier survival analysis and comparisons were performed using the log-rank test. RESULTS: Of the 615 enrolled patients, 298 (48.5%) chose primary intervention and 317 (51.5%) chose active surveillance. From the active surveillance cohort, 45 (14.2%) patients underwent delayed intervention. Median follow-up time for the entire registry was 2.9 years, with 203 (33.0%) patients followed for 5 years or more. At baseline, patients who chose active surveillance were older (P < 0.001) and had higher comorbidity status (P < 0.001) than those who chose primary intervention. There was no difference in cancer-specific survival at 7 years between primary intervention and active surveillance (99.0% vs 100%, respectively, P ¼ 0.3) [Figure 1A]. However, overall survival was higher in patients with primary intervention when compared to active surveillance at 5 years (93.0% vs 80.2%, respectively) and 7 years (91.7% vs 65.9%, respectively, P ¼ 0.002) [Figure 1B]. The 5-year and 7-year progression-free survival rate in the active surveillance cohort was 83.9% and 71.4%, respectively. CONCLUSIONS: In the intermediate-term, active surveillance appears to be as safe as and not inferior to primary intervention for carefully selected patients with small renal masses. As the registry matures, further studies will elucidate the effectiveness of active surveillance in the long-term.
e1133
trigger reflex crossover to intervention as growth rates are highly variable within the first 6-12 months of surveillance. Instead we recommend re-assessment of risk stratification with additional imaging or consideration of biopsy prior to treatment. The role of GR in decision making for SRM on AS requires further refinement.
Source of Funding: Research reported in this abstract was supported by the TL1 Predoctoral Training Program of the National Institutes of Health under award number TL1200008. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Source of Funding: National Institutes of Health (NIH), Grant Number TL1 TR001078.
PD59-02 VARIABILITY IN GROWTH KINETICS OF SMALL RENAL MASSES ON ACTIVE SURVEILLANCE: RESULTS FROM THE DISSRM REGISTRY Akachimere Uzosike*, Michael Johnson, Hiten Patel, Mark Riffon, Michael Gorin, Christian Pavlovich, Baltimore, MD; Peter Chang, Andrew Wagner, Boston, MA; Bruce Trock, Mohamad Allaf, Phillip Pierorazio, Baltimore, MD INTRODUCTION AND OBJECTIVES: Active surveillance (AS) is emerging as a safe and effective strategy for the management of small renal masses, which are defined as solid masses with a maximum diameter less than 4.0cm. We conducted this prospective multi-institutional study involving patients with small renal masses in order to characterize the growth rates of these masses and their pertinence to clinical outcomes. METHODS: Beginning in 2009, the Delayed Intervention and Surveillance for Small Renal Masses (DISSRM), a prospective multiinstitutional registry of patients with small renal masses, has enrolled patients who chose either primary intervention or AS. Patients electing active surveillance received regularly scheduled imaging, with tumor characteristics collected throughout their enrollment in the registry. RESULTS: 615 patients were prospectively enrolled, of which 317 patients (51.5%) elected AS. 284 had follow-up imaging at time of this analysis, with a mean follow-up of 2.91 years. Overall mean growth rate was -0.11 cm0.31cm/year (median: -0.07 cm/year). Growth rate and variability decreased with time, with the mean growth rates at 6, 12, 24, and 48 months of -0.100.09, -0.08 0.07, -0.050.056, and -0.040.02 cm/ year, respectively (Figure 1). GR was not predictive of adverse pathological features. No patient developed metastatic disease or died of kidney cancer. CONCLUSIONS: Growth kinetics of SRM is highly variable upon entrance into AS, with both growth rate and growth rate variability decreasing with time. Early in AS, worrisome growth rates should not
PD59-03 GROWTH KINETICS IN VON HIPPEL-LINDAU-ASSOCIATED RENAL TUMORS: DEFINING THE INFLUENCE OF GERMLINE MUTATION TYPE Mark Ball*, Shawna Boyle, Bethesda, MD; Kiranpreet Khurana, Cleveland, OH; Rabindra Gautam, Bethesda, MD; Gennady Bratslavsky, Syracuse, NY; W. Marston Linehan, Adam Metwalli, Bethesda, MD INTRODUCTION AND OBJECTIVES: Renal cell carcinoma develops in 25-60% of patients von Hippel-Lindau (VHL), which is characterized by germline mutations in the VHL gene. The paradigm for treating renal tumors in VHL includes active surveillance for lesions less than 3 cm, and surgical resection for lesions greater than 3 cm. Knowledge of growth rates for renal lesions in VHL guide surveillance schedules. While the risk of developing RCC is related to VHL genotype, it is unknown if VHL genotype can influence tumor growth rate. We sought to characterize growth rate for VHL-associated renal tumors and to determine if the type of germline mutation in VHL influences tumor growth kinetics. METHODS: Patients with solid, enhancing renal tumors with at least 3 cross sectional imaging studies and known germline mutation status were retrospectively reviewed. In patients with multiple index lesions, all lesions were analyzed. Renal tumor size was measured as the largest single-dimension diameter. Growth rates were calculated using linear regression. Germline mutations were categorized into missense, partial deletion, frameshift, deletion, splice donor, amino acid insertion, and splice acceptor. The effect of germline mutation type on renal tumor kinetics was assessed with the Wilcoxon-ranksum or Kruskall Wallis tests. RESULTS: A total of 246 tumors in 161 patients and 1341 timepoint measurements were included for analysis. Median growth rate for the entire cohort was 3.5 mm (interquartile range 2.4-5.1 mm). Median growth rates were similar for all mutation categories: 3.4 mm for missense (n¼111), 3.5 mm for partial deletion (n¼71), 3.2 mm for nonsense (n¼28), 4.5 mm for frameshift (n¼16), 2.5 mm for deletion (n¼8), 3.4 mm for splice donor (n¼4), 3.9 mm for amino acid insertion (n¼3), and 4.9 mm for splice acceptor (n¼3) (Figure 1). There was no difference in growth rates between missense and non-missense tumors (p¼0.1)