Search

Disclosure TP has received research funding from Merck Serono, Merck, Sharp & Dohme (MSD), Roche, Bristol Myers Squibb (BMS), AstraZeneca, Astellas, Novartis, Johnson and Johnson, Seattle Genetics, Pfizer, Exelixis and Eisai and honoraria from Merck Serono, MSD, Roche, BMS, AstraZeneca, Astellas, Novartis, Johnson and Johnson, Seattle Genetics, Pfizer, Exelixis and Eisai; JB has received honoraria for participation in advisory boards from Pfizer, AstraZeneca, Merck and BMS, invited speaker fees from Merck, Genentech and MSD, royalties from UpToDate, institutional research funding as principal investigator (PI) for MSD and Pfizer, research funding from Takeda and non-remunerated activities as steering committee member of the IMvigor 011 study; EC has received honoraria from Jansen for invited speaker and non-remunerated activities in an advisory role for the EAU guidelines; MDS has received honoraria for participation in advisory boards and as an invited speaker for 4D, AAA, Amgen, Astellas, AstraZeneca, Basilea, Bayer, Bioclin, BMS, EISAI, Ferring, Immunomedics, Ipsen, Janssen, MSD, Merck Serono, Novartis, Pfizer, Pierre Fabre Oncology, Roche, Sandoz, Sanofi, SeaGen and Amgen and institutional research as PI and steering committee member for Basilea, AstraZeneca, MSD, Merck, EISAI, Astellas, SeaGen, Exelixis, Ipsen, Roche, Immunomedics, Janssen and Calithera; RH has received honoraria for participation in advisory boards for Roche, Nektar, BMS, MSD and Astellas, expert testimony for National Institute of Clinical Excellence and partnership in the Cancer Centre London, institutional royalties received from Janssen, research grants from MSD and Roche, local PI for Roche, MSD, Basilea and Cancer Research UK; patient funding from Astellas and steering committee member with Cancer Research UK; YL has received honoraria for lectures, presentations, speaker’s bureau, manuscript writing or educational events from BMS, Pfizer, Merck KGaA, MSD, AstraZeneca, Roche, Jansen, Astellas, Seattle Genetics and Immunomedics and support for attending meetings and/or travel grants from BMS, Roche, AstraZeneca, MSD and Pfizer; AN has received institutional research grants from Merck, AstraZeneca, Ipsen and BMS and has undertaken personal research as a steering committee member for Roche, Janssen, Bayer, Astellas, AstraZeneca, Merck and Clovis Oncology; BPV has received honoraria for advisory boards for Pfizer, Astellas Pharma, BMS, Ipsen, EUSA Pharma, Sanofi-Aventis and Merck and has been an invited speaker for Janssen, Pfizer, BMS, Roche, Bayer, EUSA Pharma, MSD and Merck; AR has received honoraria for advisory boards for Pfizer, Merck GA, BMS, Ipsen, MSD and AstraZeneca and has been an invited speaker for Pfizer, Merck GA, BMS, Ipsen and MSD and has received institutional grants from Pfizer, Merck GA and Ipsen; SFS has received honoraria for participation in advisory boards for Astellas, Janssen, MSD, AstraZeneca, Bayer, BMS, Cepheid, Ferring Pharmaceuticals, Ipsen, Lilly, Olympus, Pfizer, Pierre Fabre, Richard Wolf, Roche, Sanochemia, Sanofi, Takeda and UroGen; BS has received honoraria from Ellipses, Ipsen, Merck, Pfizer and Roche and has received travel and research funding from BMS, Genentech, MSD, Pfizer and Roche; MSvdH has received honoraria (paid to institute) for participation in advisory boards for BMS, Roche, Seagen, AstraZeneca, Janssen, Pfizer and MSD, stock ownership with Gilead; and institutional research funding from BMS, Roche, AstraZeneca and 4SC; SG has received personal honoraria for participation in advisory boards for Sanofi, Orion, Roche, Amgen, MSD and Aranda; other honoraria from RSI Televisione Svizzera Italiana); has been an invited speaker for ESMO, SAKK, SAMO, Orikata and CACA-GU, speaker’s bureau for Janssen Cilag; travel grant from ProteoMEdiX, institutional honoraria for advisory boards for Bayer, Janssen Cilag, Roche and AAA International including Independent Data Monitoring Committee; steering committee for Amgen, Menarini Silicon Biosystems, Astellas Pharma, Tolero Pharmaceuticals, MSD, Pfizer, Telixpharma, BMS and Orion and has received a patent, royalties and other intellectual property from Method for Biomarker WO2009138392.

Background: To test the effect of variant histology relative to urothelial histology on stage at presentation, cancer specific mortality (CSM), and overall mortality (OM) after chemotherapy use, in urethral cancer. Materials and Methods: Within the Surveillance, Epidemiology and End Results (2004–2016) database, we identified 1,907 primary variant histology urethral cancer patients. Kaplan-Meier plots, Cox regression analyses, cumulative incidence-plots, multivariable competing-risks regression models and propensity score matching for patient and tumor characteristics were used. Results: Of 1,907 eligible urethral cancer patients, urothelial histology affected 1,009 (52.9%) vs. squamous cell carcinoma (SCC) 455 (23.6%) vs. adenocarcinoma 278 (14.6%) vs. other histology 165 (8.7%) patients. Urothelial histological patients exhibited lower stages at presentation than SCC, adenocarcinoma or other histology patients. In urothelial histology patients, five-year CSM was 23.5% vs. 34.4% in SCC [Hazard Ratio (HR) 1.57] vs. 40.7% in adenocarcinoma (HR 1.69) vs. 43.4% in other histology (HR 1.99, p < 0.001). After matching in multivariate competing-risks regression models, variant histology exhibited 1.35-fold higher CSM than urothelial. Finally, in metastatic urethral cancer, lower OM was recorded after chemotherapy in general, including metastatic adenocarcinoma and other variant histology subtypes, except metastatic SCC. Conclusion: Adenocarcinoma, SCC and other histology subtypes affect fewer patients than urothelial histology. Presence of variant histology results in higher CSM. Finally, chemotherapy for metastatic urethral cancer improves survival in adenocarcinoma and other variant histology subtypes, but not in SCC.

Adjuvant Nivolumab for Invasive Urothelial Carcinoma In a prospective, randomized trial involving patients with urothelial carcinoma who had undergone radical surgery, adjuvant nivolumab was compared with placebo. The median disease-free survival was 20.8 months with nivolumab and 10.8 months with placebo. Treatment-related adverse events of grade 3 or higher were noted in 17.9% of patients in the nivolumab group. Background The role of adjuvant treatment in high-risk muscle-invasive urothelial carcinoma after radical surgery is not clear. Methods In a phase 3, multicenter, double-blind, randomized, controlled trial, we assigned patients with muscle-invasive urothelial carcinoma who had undergone radical surgery to receive, in a 1:1 ratio, either nivolumab (240 mg intravenously) or placebo every 2 weeks for up to 1 year. Neoadjuvant cisplatin-based chemotherapy before trial entry was allowed. The primary end points were disease-free survival among all the patients (intention-to-treat population) and among patients with a tumor programmed death ligand 1 (PD-L1) expression level of 1% or more. Survival free from recurrence outside the urothelial tract was a secondary end point. Results A total of 353 patients were assigned to receive nivolumab and 356 to receive placebo. The median disease-free survival in the intention-to-treat population was 20.8 months (95% confidence interval [CI], 16.5 to 27.6) with nivolumab and 10.8 months (95% CI, 8.3 to 13.9) with placebo. The percentage of patients who were alive and disease-free at 6 months was 74.9% with nivolumab and 60.3% with placebo (hazard ratio for disease recurrence or death, 0.70; 98.22% CI, 0.55 to 0.90; P

Introduction and objectives: The goals of transurethral resection of a bladder tumor (TUR) are to completely resect the lesions and to make a correct diagnosis in order to adequately stage the patient. It is well known that the presence of detrusor muscle in the specimen is a prerequisite to minimize the risk of under staging. Persistent disease after resection of bladder tumors is not uncommon and is the reason why the European Guidelines recommended a re-TUR for all T1 tumors. It was recently published that when there is muscle in the specimen, re-TUR does not influence progression or cancer specific survival. We present here the patient and tumor factors that may influence the presence of residual disease at re-TUR. Material and methods: In our retrospective cohort of 2451 primary T1G3 patients initially treated with BCG, pathology results for 934 patients (38.1%) who underwent re-TUR are available. 74% had multifocal tumors, 20% of tumors were more than 3 cm in diameter and 26% had concomitant CIS. In this subgroup of patients who underwent re-TUR, there was no residual disease in 267 patients (29%) and residual disease in 667 patients (71%): Ta in 378 (40%) and T1 in 289 (31%) patients. Age, gender, tumor status (primary/recurrent), previous intravesical therapy, tumor size, tumor multi-focality, presence of concomitant CIS, and muscle in the specimen were analyzed in order to evaluate risk factors of residual disease at re-TUR, both in univariate analyses and multivariate logistic regressions. Results: The following were not risk factors for residual disease: age, gender, tumor status and previous intravesical chemotherapy. The following were univariate risk factors for presence of residual disease: no muscle in TUR, multiple tumors, tumors >= 3 cm, and presence of concomitant CIS. Due to the correlation between tumor multi-focality and tumor size, the multivariate model retained either the number of tumors or the tumor diameter (but not both), p < 0.001. The presence of muscle in the specimen was no longer significant, while the presence of CIS only remained significant in the model with tumor size, p < 0.001. Conclusions: The most significant factors for a higher risk of residual disease at re-TUR in T1G3 patients are multifocal tumors and tumors more than 3 cm. Patients with concomitant CIS and those without muscle in the specimen also have a higher risk of residual disease. (C) 2021 AEU. Published by Elsevier Espana, S.L.U. All rights reserved.

Objective: To examine the incidence and time trends of secondary bladder cancer (BCa) and rectal cancer (RCa) after brachytherapy (BT) relative to radical prostatectomy (RP). Materials and Methods: Within the Surveillance, Epidemiology and End Results (SEER) database (1988–2015), we identified patients with localized PCa as an only or first primary cancer, who underwent BT or RP. Cumulative incidence plots and multivariable competing-risks regression (CRR) models were used. Sensitivity analyses focused on patients’ age and year of diagnosis intervals and tested the effect of an unmeasured confounder. Results: Of 318058 patients with localized prostate cancer (PCa), 55566 (18.4%) underwent BT. After propensity score-matching, 20-year secondary BCa incidence was 6.0% in patients who had undergone BT vs 2.4% in those who had undergone RP (P < 0.001) and the respective 20-year secondary RCa incidence was 1.1% vs 0.5% (P < 0.001). In multivariable CRR models, BT predicted higher secondary BCa (hazard ratio [HR] 1.58; P < 0.001) and RCa rates (HR 1.59; P < 0.001) vs RP. Sensitivity analyses replicated the same results after stratification according to age and showed HRs of decreasing magnitude for historical, intermediate and contemporary years of diagnosis. An unmeasured confounder with an HR of 2 would render the effect of BT statistically insignificant if it affected patients in the RP group with a ratio of 2 relative to those in the BT group. Finally, temporal trends showed a decrease of secondary 5-year BCa and RCa rates.>. Conclusions: Brachytherapy predominantly increases the risk of secondary BCa and, to a lesser extent, that of RCa. Follow-up of such patients is therefore required. It is encouraging that both secondary BCa, and RCa rates, in particular, have recently decreased, RCa.

Background: Renal cell carcinoma forming a venous tumor thrombus (VTT) in the inferior vena cava (IVC) has a poor prognosis. Recent investigations have been focused on prognostic markers of survival. Thrombus consistency (TC) has been proposed to be of significant value but yet there are conflicting data. The aim of this study is to test the effect of IVC VTT consistency on cancer specific survival (CSS) in a multi-institutional cohort. Methods: The records of 413 patients collected by the International Renal Cell Carcinoma–Venous Thrombus Consortium were retrospectively analyzed. All patients underwent radical nephrectomy and tumor thrombectomy. Kaplan–Meier estimate and Cox regression analyses investigated the impact of TC on CSS in addition to established clinicopathological predictors. Results: VTT was solid in 225 patients and friable in 188 patients. Median CSS was 50 months in solid and 45 months in friable VTT. TC showed no significant association with metastatic spread, pT stage, perinephric fat invasion, and higher Fuhrman grade. Survival analysis and Cox regression rejected TC as prognostic marker for CSS. Conclusions: In the largest cohort published so far, TC seems not to be independently associated with survival in RCC patients and should therefore not be included in risk stratification models. J. Surg. Oncol. 2016;114:764–768. © 2016 Wiley Periodicals, Inc.

Collecting duct renal cell carcinoma is a rare, aggressive histological subtype of renal cell carcinoma. Since few groups have evaluated the oncological prognosis in these patients based on clinical and pathological parameters, we assessed parameters prognostic for disease specific mortality.From a cohort of 14,047 patients with renal cell carcinoma we retrieved the records of 95 with collecting duct renal cell carcinoma at a total of 16 European and American centers of the CORONA (Collaborative Research on Renal Neoplasms Association) and SATURN (Surveillance and Treatment Update Renal Neoplasms) projects, and another 2 centers. Multivariable Cox regression analysis was applied to determine the influence of parameters on disease specific mortality. Median followup was 48.1 months (IQR 24-103).The disease specific survival rate at 1, 2, 5 and 10 years was 60.4%, 47.3%, 40.3% and 32.8%, respectively. American Society of Anesthesiologists (ASA) score 3-4, tumor size greater than 7 cm, stage M1, Fuhrman grade 3-4 and lymphovascular invasion independently predicted disease specific mortality. Based on these parameters, patients were divided into 26 (27%) at low, 13 (14%) at intermediate and 56 (59%) at high risk with a 5-year disease specific survival rate of 96%, 62% and 8%, respectively (bootstrap corrected c-index 0.894, 95% CI 0.820-0.967, p0.001).While patients with collecting duct renal cell carcinoma are commonly diagnosed at advanced stage and have poor prognosis after surgery, a subset has excellent survival. Histopathological features can help risk stratify patients based on the described, highly accurate risk model to predict disease specific mortality, facilitating patient counseling and risk based clinical decision making for adjuvant therapy and clinical trial inclusion.