2,255 results on '"Kantoff, Philip"'
Search Results
2. The Impact of Androgen Deprivation Therapy on COVID-19 Illness in Men With Prostate Cancer
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Shah, Neil J, Patel, Vaibhav G, Zhong, Xiaobo, Pina, Luis, Hawley, Jessica E, Lin, Emily, Gartrell, Benjamin A, Febles, Victor Adorno, Wise, David R, Qin, Qian, Mellgard, George, Joshi, Himanshu, Nauseef, Jones T, Green, David A, Vlachostergios, Panagiotis J, Kwon, Daniel H, Huang, Franklin, Liaw, Bobby, Tagawa, Scott, Kantoff, Philip, Morris, Michael J, and Oh, William K
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Aging ,Urologic Diseases ,Patient Safety ,Clinical Research ,Prevention ,Cancer ,Prostate Cancer ,Lung ,Good Health and Well Being ,Aged ,Androgen Antagonists ,Androgens ,COVID-19 ,COVID-19 Testing ,Humans ,Male ,Prostatic Neoplasms ,Receptors ,Androgen ,Retrospective Studies ,SARS-CoV-2 ,COVID-19 Drug Treatment - Abstract
BackgroundTMPRSS2, a cell surface protease regulated by androgens and commonly upregulated in prostate cancer (PCa), is a necessary component for SARS-CoV-2 viral entry into respiratory epithelial cells. Previous reports suggested a lower risk of SARS-CoV-2 among PCa patients on androgen deprivation therapy (ADT). However, the impact of ADT on severe COVID-19 illness is poorly understood.MethodsWe performed a multicenter study across 7 US medical centers and evaluated patients with PCa and SARS-CoV-2 detected by polymerase-chain-reaction between March 1, 2020, and May 31, 2020. PCa patients were considered on ADT if they had received appropriate ADT treatment within 6 months of COVID-19 diagnosis. We used multivariable logistic and Cox proportional-hazard regression models for analysis. All statistical tests were 2-sided.ResultsWe identified 465 PCa patients (median age = 71 years) with a median follow-up of 60 days. Age, body mass index, cardiovascular comorbidity, and PCa clinical disease state adjusted overall survival (hazard ratio [HR] = 1.16, 95% confidence interval [CI] = 0.68 to 1.98, P = .59), hospitalization status (HR = 0.96, 95% CI = 0.52 to 1.77, P = .90), supplemental oxygenation (HR 1.14, 95% CI = 0.66 to 1.99, P = .64), and use of mechanical ventilation (HR = 0.81, 95% CI = 0.25 to 2.66, P = .73) were similar between ADT and non-ADT cohorts. Similarly, the addition of androgen receptor-directed therapy within 30 days of COVID-19 diagnosis to ADT vs ADT alone did not statistically significantly affect overall survival (androgen receptor-directed therapy: HR = 1.27, 95% CI = 0.69 to 2.32, P = .44).ConclusionsIn this retrospective cohort of PCa patients, the use of ADT was not demonstrated to influence severe COVID-19 outcomes, as defined by hospitalization, supplemental oxygen use, or death. Age 70 years and older was statistically significantly associated with a higher risk of developing severe COVID-19 disease.
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- 2022
3. Refining Risk Stratification of High-risk and Locoregional Prostate Cancer: A Pooled Analysis of Randomized Trials
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Ravi, Praful, Xie, Wanling, Buyse, Marc, Halabi, Susan, Kantoff, Philip W., Sartor, Oliver, Attard, Gert, Clarke, Noel, D'Amico, Anthony, Dignam, James, James, Nicholas, Fizazi, Karim, Gillessen, Silke, Parulekar, Wendy, Sandler, Howard, Spratt, Daniel E., Sydes, Matthew R., Tombal, Bertrand, Williams, Scott, and Sweeney, Christopher J.
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- 2024
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4. Benchmarks for Academic Oncology Faculty.
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Anthony, Lowell, Atweh, George, Bhatia, Ravi, Carey, Lisa A, Chang, Jenny C, Edelman, Martin J, Kantoff, Philip W, Markham, Merry Jennifer, Messersmith, Wells, Nelson, Edward L, Oettel, Kurt, O'Regan, Ruth, Verschraegen, Claire F, and Vose, Julie M
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Biomedical and Clinical Sciences ,Oncology and Carcinogenesis ,Cancer ,6.9 Resources and infrastructure (treatment evaluation) ,Evaluation of treatments and therapeutic interventions ,Benchmarking ,Faculty ,Medical ,Humans ,Leadership ,Medical Oncology ,Research Personnel ,Oncology and carcinogenesis - Abstract
The role of clinical researchers is vital to cancer progress. The teaching, research, and leadership roles that academic oncologists hold need to be accounted for and appropriately compensated. National metrics are currently inexistent, but are necessary to move the oncology research field forward. Clinical research and routine clinical care must be harmoniously integrated without competing. This article reviews the national landscape of clinical cancer research and proposes a call for action.
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- 2021
5. Survival of African-American and Caucasian men after sipuleucel-T immunotherapy: outcomes from the PROCEED registry
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Sartor, Oliver, Armstrong, Andrew J, Ahaghotu, Chiledum, McLeod, David G, Cooperberg, Matthew R, Penson, David F, Kantoff, Philip W, Vogelzang, Nicholas J, Hussain, Arif, Pieczonka, Christopher M, Shore, Neal D, Quinn, David I, Small, Eric J, Heath, Elisabeth I, Tutrone, Ronald F, Schellhammer, Paul F, Harmon, Matthew, Chang, Nancy N, Sheikh, Nadeem A, Brown, Bruce, Freedland, Stephen J, and Higano, Celestia S
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Cancer ,Prostate Cancer ,Urologic Diseases ,Adult ,Black or African American ,Aged ,Aged ,80 and over ,Cancer Vaccines ,Disease Progression ,Follow-Up Studies ,Health Status Disparities ,Humans ,Infusions ,Intravenous ,Kallikreins ,Kaplan-Meier Estimate ,Male ,Middle Aged ,Prostate-Specific Antigen ,Prostatic Neoplasms ,Castration-Resistant ,Registries ,Time Factors ,Tissue Extracts ,Treatment Outcome ,White People ,Oncology and Carcinogenesis ,Urology & Nephrology - Abstract
PurposeAfrican Americans experience greater prostate cancer risk and mortality than do Caucasians. An analysis of pooled phase III data suggested differences in overall survival (OS) between African American and Caucasian men receiving sipuleucel-T. We explored this in PROCEED (NCT01306890), an FDA-requested registry in over 1900 patients with metastatic castration-resistant prostate cancer (mCRPC) treated with sipuleucel-T.Patients and methodsOS for patients who received ≥1 sipuleucel-T infusion was compared between African American and Caucasian men using an all patient set and a baseline prostate-specific antigen (PSA)-matched set (two Caucasians to every one African American with baseline PSAs within 10% of each other). Univariable and multivariable analyses were conducted. Survival data were examined using Kaplan-Meier and Cox proportional hazard methodologies.ResultsMedian follow-up was 46.6 months. Overall survival differed between African American and Caucasian men with hazard ratios (HR) of 0.81 (95% confidence interval [CI]: 0.68-0.97, P = 0.03) in the all patient set and 0.70 (95% CI: 0.57-0.86, P
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- 2020
6. Family history of prostate cancer and the incidence of ERG- and phosphatase and tensin homolog-defined prostate cancer.
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Hashim, Dana, Gonzalez-Feliciano, Amparo, Ahearn, Thomas, Pettersson, Andreas, Barber, Lauren, Pernar, Claire, Ebot, Ericka, Finn, Stephen, Giovannucci, Edward, Lis, Rosina, Loda, Massimo, Parmigiani, Giovanni, Lotan, Tamara, Kantoff, Philip, Mucci, Lorelei, Graff, Rebecca, and Isikbay, Masis
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PTEN ,TMPRSS2:ERG ,family history ,molecular subtypes ,prostate cancer ,Adult ,Aged ,Biomarkers ,Tumor ,Cohort Studies ,Genetic Predisposition to Disease ,Humans ,Incidence ,Male ,Middle Aged ,PTEN Phosphohydrolase ,Prostatic Neoplasms ,Risk Factors ,Transcriptional Regulator ERG - Abstract
Family history is among the strongest known risk factors for prostate cancer (PCa). Emerging data suggest molecular subtypes of PCa, including two somatic genetic aberrations: fusions of androgen-regulated promoters with ERG and, separately, phosphatase and tensin homolog (PTEN) loss. We examined associations between family history and incidence of these subtypes in 44,126 men from the prospective Health Professionals Follow-up Study. ERG and PTEN status were assessed by immunohistochemistry. Multivariable competing risks models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for associations between self-reported family history of PCa and molecular subtypes of disease. Thirteen percent of men had a positive family history of PCa at baseline. During a median follow-up of 18.5 years, 5,511 PCa cases were diagnosed. Among them, 888 were assayed for ERG status (47% ERG-positive) and 715 were assayed for PTEN loss (14% PTEN null). Family history was more strongly associated with risk of ERG-negative (HR: 2.15; 95% CI: 1.71-2.70) than ERG-positive (HR: 1.49; 95% CI: 1.13-1.95) disease (pheterogeneity : 0.04). The strongest difference was among men with an affected father (HRERG-negative : 2.09; 95% CI: 1.64-2.66; HRERG-positive : 1.30; 95% CI: 0.96-1.76; pheterogeneity : 0.01). Family history of PCa was positively associated with both PTEN null (HR: 2.10; 95% CI: 1.26-3.49) and PTEN intact (HR: 1.72; 95% CI: 1.39-2.13) PCa (pheterogeneity : 0.47). Our results indicate that PCa family history may be positively associated with PCa in all ERG and PTEN subtypes, suggesting a role of genetic susceptibility in their development. It is possible that ERG-negative disease could be especially associated with positive family history.
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- 2020
7. Management of Patients with Advanced Prostate Cancer: Report of the Advanced Prostate Cancer Consensus Conference 2019
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Gillessen, Silke, Attard, Gerhardt, Beer, Tomasz M, Beltran, Himisha, Bjartell, Anders, Bossi, Alberto, Briganti, Alberto, Bristow, Rob G, Chi, Kim N, Clarke, Noel, Davis, Ian D, de Bono, Johann, Drake, Charles G, Duran, Ignacio, Eeles, Ros, Efstathiou, Eleni, Evans, Christopher P, Fanti, Stefano, Feng, Felix Y, Fizazi, Karim, Frydenberg, Mark, Gleave, Martin, Halabi, Susan, Heidenreich, Axel, Heinrich, Daniel, Higano, Celestia Tia S, Hofman, Michael S, Hussain, Maha, James, Nicolas, Kanesvaran, Ravindran, Kantoff, Philip, Khauli, Raja B, Leibowitz, Raya, Logothetis, Chris, Maluf, Fernando, Millman, Robin, Morgans, Alicia K, Morris, Michael J, Mottet, Nicolas, Mrabti, Hind, Murphy, Declan G, Murthy, Vedang, Oh, William K, Ost, Piet, O'Sullivan, Joe M, Padhani, Anwar R, Parker, Chris, Poon, Darren MC, Pritchard, Colin C, Reiter, Robert E, Roach, Mack, Rubin, Mark, Ryan, Charles J, Saad, Fred, Sade, Juan Pablo, Sartor, Oliver, Scher, Howard I, Shore, Neal, Small, Eric, Smith, Matthew, Soule, Howard, Sternberg, Cora N, Steuber, Thomas, Suzuki, Hiroyoshi, Sweeney, Christopher, Sydes, Matthew R, Taplin, Mary-Ellen, Tombal, Bertrand, Türkeri, Levent, van Oort, Inge, Zapatero, Almudena, and Omlin, Aurelius
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Cancer ,Urologic Diseases ,Aging ,Prostate Cancer ,Good Health and Well Being ,Bone Neoplasms ,Humans ,Male ,Neoplasm Metastasis ,Neoplasm Recurrence ,Local ,Neoplasm Staging ,Practice Guidelines as Topic ,Prostate-Specific Antigen ,Prostatic Neoplasms ,Advanced prostate cancer ,High-risk localised prostate cancer ,Hormone-sensitive prostate cancer ,Castration-resistant prostate cancer ,Oligometastatic prostate cancer ,Progression-free survival ,Overall survival ,Prostate cancer treatment ,Imaging ,Genetics ,Tumour genomic profiling ,Castration-naïve prostate cancer ,Clinical Sciences ,Urology & Nephrology - Abstract
BackgroundInnovations in treatments, imaging, and molecular characterisation in advanced prostate cancer have improved outcomes, but there are still many aspects of management that lack high-level evidence to inform clinical practice. The Advanced Prostate Cancer Consensus Conference (APCCC) 2019 addressed some of these topics to supplement guidelines that are based on level 1 evidence.ObjectiveTo present the results from the APCCC 2019.Design, setting, and participantsSimilar to prior conferences, experts identified 10 important areas of controversy regarding the management of advanced prostate cancer: locally advanced disease, biochemical recurrence after local therapy, treating the primary tumour in the metastatic setting, metastatic hormone-sensitive/naïve prostate cancer, nonmetastatic castration-resistant prostate cancer, metastatic castration-resistant prostate cancer, bone health and bone metastases, molecular characterisation of tissue and blood, inter- and intrapatient heterogeneity, and adverse effects of hormonal therapy and their management. A panel of 72 international prostate cancer experts developed the programme and the consensus questions.Outcome measurements and statistical analysisThe panel voted publicly but anonymously on 123 predefined questions, which were developed by both voting and nonvoting panel members prior to the conference following a modified Delphi process.Results and limitationsPanellists voted based on their opinions rather than a standard literature review or formal meta-analysis. The answer options for the consensus questions had varying degrees of support by the panel, as reflected in this article and the detailed voting results reported in the Supplementary material.ConclusionsThese voting results from a panel of prostate cancer experts can help clinicians and patients navigate controversial areas of advanced prostate management for which high-level evidence is sparse. However, diagnostic and treatment decisions should always be individualised based on patient-specific factors, such as disease extent and location, prior lines of therapy, comorbidities, and treatment preferences, together with current and emerging clinical evidence and logistic and economic constraints. Clinical trial enrolment for men with advanced prostate cancer should be strongly encouraged. Importantly, APCCC 2019 once again identified important questions that merit assessment in specifically designed trials.Patient summaryThe Advanced Prostate Cancer Consensus Conference provides a forum to discuss and debate current diagnostic and treatment options for patients with advanced prostate cancer. The conference, which has been held three times since 2015, aims to share the knowledge of world experts in prostate cancer management with health care providers worldwide. At the end of the conference, an expert panel discusses and votes on predefined consensus questions that target the most clinically relevant areas of advanced prostate cancer treatment. The results of the voting provide a practical guide to help clinicians discuss therapeutic options with patients as part of shared and multidisciplinary decision making.
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- 2020
8. Real‐world outcomes of sipuleucel‐T treatment in PROCEED, a prospective registry of men with metastatic castration‐resistant prostate cancer
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Higano, Celestia S, Armstrong, Andrew J, Sartor, A Oliver, Vogelzang, Nicholas J, Kantoff, Philip W, McLeod, David G, Pieczonka, Christopher M, Penson, David F, Shore, Neal D, Vacirca, Jeffrey, Concepcion, Raoul S, Tutrone, Ronald F, Nordquist, Luke T, Quinn, David I, Kassabian, Vahan, Scholz, Mark C, Harmon, Matt, Tyler, Robert C, Chang, Nancy N, Tang, Hong, and Cooperberg, Matthew R
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Biomedical and Clinical Sciences ,Clinical Sciences ,Oncology and Carcinogenesis ,Cancer ,Prostate Cancer ,Urologic Diseases ,Aging ,Evaluation of treatments and therapeutic interventions ,6.1 Pharmaceuticals ,Aged ,Humans ,Male ,Neoplasm Metastasis ,Prospective Studies ,Prostatic Neoplasms ,Castration-Resistant ,Registries ,Tissue Extracts ,immunotherapy ,overall survival ,prostate cancer ,safety ,Public Health and Health Services ,Oncology & Carcinogenesis ,Oncology and carcinogenesis ,Public health - Abstract
BackgroundThe large registry, PROVENGE Registry for the Observation, Collection, and Evaluation of Experience Data (PROCEED)(NCT01306890), evaluated sipuleucel-T immunotherapy for asymptomatic/minimally symptomatic metastatic castration-resistant prostate cancer (mCRPC).MethodsPROCEED enrolled patients with mCRPC receiving 3 biweekly sipuleucel-T infusions. Assessments included overall survival (OS), serious adverse events (SAEs), cerebrovascular events (CVEs), and anticancer interventions (ACIs). Follow-up was for ≥3 years or until death or study withdrawal.ResultsIn 2011-2017, 1976 patients were followed for 46.6 months (median). The median age was 72 years, and the baseline median prostate-specific antigen level was 15.0 ng/mL; 86.7% were white, and 11.6% were African American. Among the patients, 1902 had 1 or more sipuleucel-T infusions. The median OS was 30.7 months (95% confidence interval [CI], 28.6-32.2 months). Known prognostic factors were independently associated with OS in a multivariable analysis. Among the 1255 patients who died, 964 (76.8%) died of prostate cancer (PC) progression. The median time from the first infusion to PC death was 42.7 months (95% CI, 39.4-46.2 months). The incidence of sipuleucel-T-related SAEs was 3.9%. The incidence of CVEs was 2.8%, and the rate per 100 person-years was 1.2 (95% CI, 0.9-1.6). The CVE incidence among 11,972 patients with mCRPC from the Surveillance, Epidemiology, and End Results-Medicare database was 2.8%; the rate per 100 person-years was 1.5 (95% CI, 1.4-1.7). One or more ACIs (abiraterone, enzalutamide, docetaxel, cabazitaxel, or radium 223) were received by 77.1% of the patients after sipuleucel-T; 32.5% and 17.4% of the patients experienced 1- and 2-year treatment-free intervals, respectively.ConclusionsPROCEED provides contemporary survival data for sipuleucel-T-treated men in a real-world setting of new life-prolonging agents, which will be useful in discussing treatment options with patients and in powering future trials with sipuleucel-T. The safety and tolerability of sipuleucel-T in PROCEED were consistent with previous findings.
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- 2019
9. Characterising the contribution of rare protein-coding germline variants to prostate cancer risk and severity in 37,184 cases
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Mitchell, Jonathan, primary, Camacho, Niedzica, additional, Shea, Patrick, additional, Stopsack, Konrad, additional, Joseph, Vijai, additional, Burren, Oliver Simon, additional, Dhindsa, Ryan, additional, Nag, Abhishek, additional, Berchuck, Jacob, additional, O'Neill, Amanda, additional, Abbasi, Ali, additional, Zoghbi, Anthony, additional, Alegre-Diaz, Jesus, additional, Kuri-Morales, Pablo, additional, Berumen, Jaime, additional, Tapia-Conyer, Roberto, additional, Emberson, Jonathan, additional, Torres, Jason, additional, Collins, Rory, additional, Wang, Quanli, additional, Goldstein, David, additional, Matakidou, Athena, additional, Haefliger, Carolina, additional, Anderson-Dring, Lauren, additional, March, Ruth, additional, Jobanputra, Vaidehi, additional, Dougherty, Brian, additional, Carss, Keren, additional, Petrovski, Slave, additional, Kantoff, Philip, additional, Offit, Kenneth, additional, Mucci, Lorelei, additional, Pomerantz, Mark, additional, and Fabre, Margarete, additional
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- 2024
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10. Novel RB1-Loss Transcriptomic Signature Is Associated with Poor Clinical Outcomes across Cancer Types
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Chen, William S, Alshalalfa, Mohammed, Zhao, Shuang G, Liu, Yang, Mahal, Brandon A, Quigley, David A, Wei, Ting, Davicioni, Elai, Rebbeck, Timothy R, Kantoff, Philip W, Maher, Christopher A, Knudsen, Karen E, Small, Eric J, Nguyen, Paul L, and Feng, Felix Y
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Rare Diseases ,Genetics ,Human Genome ,Clinical Research ,Cancer ,Good Health and Well Being ,Biomarkers ,Tumor ,Disease Progression ,Humans ,Male ,Neoplasms ,Prognosis ,Transcriptome ,Oncology and Carcinogenesis ,Oncology & Carcinogenesis - Abstract
PurposeRb-pathway disruption is of great clinical interest, as it has been shown to predict outcomes in multiple cancers. We sought to develop a transcriptomic signature for detecting biallelic RB1 loss (RBS) that could be used to assess the clinical implications of RB1 loss on a pan-cancer scale.Experimental designWe utilized data from the Cancer Cell Line Encyclopedia (N = 995) to develop the first pan-cancer transcriptomic signature for predicting biallelic RB1 loss (RBS). Model accuracy was validated using The Cancer Genome Atlas (TCGA) Pan-Cancer dataset (N = 11,007). RBS was then used to assess the clinical relevance of biallelic RB1 loss in TCGA Pan-Cancer and in an additional metastatic castration-resistant prostate cancer (mCRPC) cohort.ResultsRBS outperformed the leading existing signature for detecting RB1 biallelic loss across all cancer types in TCGA Pan-Cancer (AUC, 0.89 vs. 0.66). High RBS (RB1 biallelic loss) was associated with promoter hypermethylation (P = 0.008) and gene body hypomethylation (P = 0.002), suggesting RBS could detect epigenetic gene silencing. TCGA Pan-Cancer clinical analyses revealed that high RBS was associated with short progression-free (P < 0.00001), overall (P = 0.0004), and disease-specific (P < 0.00001) survival. On multivariable analyses, high RBS was predictive of shorter progression-free survival in TCGA Pan-Cancer (P = 0.03) and of shorter overall survival in mCRPC (P = 0.004) independently of the number of DNA alterations in RB1.ConclusionsOur study provides the first validated tool to assess RB1 biallelic loss across cancer types based on gene expression. RBS can be useful for analyzing datasets with or without DNA-sequencing results to investigate the emerging prognostic and treatment implications of Rb-pathway disruption.See related commentary by Choudhury and Beltran, p. 4199.
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- 2019
11. Prognostic and therapeutic significance of COP9 signalosome subunit CSN5 in prostate cancer
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Mazzu, Ying Z., Liao, Yu-Rou, Nandakumar, Subhiksha, Jehane, Lina E., Koche, Richard P., Rajanala, Sai Harisha, Li, Ruifang, Zhao, HuiYong, Gerke, Travis A., Chakraborty, Goutam, Lee, Gwo-Shu Mary, Nanjangud, Gouri J., Gopalan, Anuradha, Chen, Yu, and Kantoff, Philip W.
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- 2022
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12. A prospective study of aspirin use and prostate cancer risk by TMPRSS2:ERG status
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Stopsack, Konrad H, Gonzalez-Feliciano, Amparo G, Peisch, Samuel F, Downer, Mary K, Gage, Riley A, Finn, Stephen, Lis, Rosina T, Graff, Rebecca E, Pettersson, Andreas, Pernar, Claire H, Loda, Massimo, Kantoff, Philip W, Ahearn, Thomas U, and Mucci, Lorelei A
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Biomedical and Clinical Sciences ,Health Sciences ,Clinical Sciences ,Oncology and Carcinogenesis ,Clinical Research ,Prevention ,Prostate Cancer ,Genetics ,Urologic Diseases ,Cancer ,Aging ,Aetiology ,2.1 Biological and endogenous factors ,Good Health and Well Being ,Adult ,Aged ,Anti-Inflammatory Agents ,Non-Steroidal ,Aspirin ,Follow-Up Studies ,Humans ,Incidence ,Male ,Middle Aged ,Oncogene Proteins ,Fusion ,Prognosis ,Prospective Studies ,Prostatic Neoplasms ,United States ,Transdisciplinary Prostate Cancer Partnership ,Medical and Health Sciences ,Epidemiology ,Biomedical and clinical sciences ,Health sciences - Abstract
Background: In a case-control study, aspirin use was associated with a lower risk of a common prostate cancer molecular subtype, the TMPRSS2:ERG gene fusion. We sought to validate this finding in a prospective cohort.Methods: In the Health Professionals Follow-up Study, 49,395 men reported on aspirin use on biennial questionnaires and were followed for prostate cancer incidence over 23 years. TMPRSS2:ERG status was assessed by IHC for presence of ERG on archival tumor specimens for 912 patients with prostate cancer, of whom 48% were ERG-positive.Results: In multivariable models, we found no association between regular use of aspirin and risk of ERG-positive prostate cancer (HR, 1.02; 95% confidence interval, 0.85-1.23), nor any association with duration or frequency of aspirin use. In restricting to cases with either high Gleason grade or advanced stage disease, there remained no association with aspirin use.Conclusions: Data from this prospective study with repeated assessments of aspirin use do not support the hypothesis that aspirin use is associated with a lower risk of ERG-positive prostate cancer.Impact: Aspirin use is unlikely to lower the risk of this common molecular subtype of prostate cancer. However, there is emerging data supporting the role of other lifestyle and genetic factors underlying the development of the TMPRSS2:ERG fusion. Cancer Epidemiol Biomarkers Prev; 27(10); 1231-3. ©2018 AACR.
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- 2018
13. Role of Genetic Testing for Inherited Prostate Cancer Risk: Philadelphia Prostate Cancer Consensus Conference 2017.
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Giri, Veda N, Knudsen, Karen E, Kelly, William K, Abida, Wassim, Andriole, Gerald L, Bangma, Chris H, Bekelman, Justin E, Benson, Mitchell C, Blanco, Amie, Burnett, Arthur, Catalona, William J, Cooney, Kathleen A, Cooperberg, Matthew, Crawford, David E, Den, Robert B, Dicker, Adam P, Eggener, Scott, Fleshner, Neil, Freedman, Matthew L, Hamdy, Freddie C, Hoffman-Censits, Jean, Hurwitz, Mark D, Hyatt, Colette, Isaacs, William B, Kane, Christopher J, Kantoff, Philip, Karnes, R Jeffrey, Karsh, Lawrence I, Klein, Eric A, Lin, Daniel W, Loughlin, Kevin R, Lu-Yao, Grace, Malkowicz, S Bruce, Mann, Mark J, Mark, James R, McCue, Peter A, Miner, Martin M, Morgan, Todd, Moul, Judd W, Myers, Ronald E, Nielsen, Sarah M, Obeid, Elias, Pavlovich, Christian P, Peiper, Stephen C, Penson, David F, Petrylak, Daniel, Pettaway, Curtis A, Pilarski, Robert, Pinto, Peter A, Poage, Wendy, Raj, Ganesh V, Rebbeck, Timothy R, Robson, Mark E, Rosenberg, Matt T, Sandler, Howard, Sartor, Oliver, Schaeffer, Edward, Schwartz, Gordon F, Shahin, Mark S, Shore, Neal D, Shuch, Brian, Soule, Howard R, Tomlins, Scott A, Trabulsi, Edouard J, Uzzo, Robert, Vander Griend, Donald J, Walsh, Patrick C, Weil, Carol J, Wender, Richard, and Gomella, Leonard G
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Humans ,Prostatic Neoplasms ,Genetic Predisposition to Disease ,Prognosis ,Risk Factors ,Predictive Value of Tests ,Pedigree ,Age Factors ,Heredity ,Phenotype ,Adult ,Aged ,Middle Aged ,Male ,Genetic Testing ,Biomarkers ,Tumor ,Clinical Decision-Making ,Genetics ,Aging ,Cancer ,Prevention ,Prostate Cancer ,Urologic Diseases ,4.1 Discovery and preclinical testing of markers and technologies ,Detection ,screening and diagnosis ,Clinical Sciences ,Oncology and Carcinogenesis ,Oncology & Carcinogenesis - Abstract
Purpose Guidelines are limited for genetic testing for prostate cancer (PCA). The goal of this conference was to develop an expert consensus-driven working framework for comprehensive genetic evaluation of inherited PCA in the multigene testing era addressing genetic counseling, testing, and genetically informed management. Methods An expert consensus conference was convened including key stakeholders to address genetic counseling and testing, PCA screening, and management informed by evidence review. Results Consensus was strong that patients should engage in shared decision making for genetic testing. There was strong consensus to test HOXB13 for suspected hereditary PCA, BRCA1/2 for suspected hereditary breast and ovarian cancer, and DNA mismatch repair genes for suspected Lynch syndrome. There was strong consensus to factor BRCA2 mutations into PCA screening discussions. BRCA2 achieved moderate consensus for factoring into early-stage management discussion, with stronger consensus in high-risk/advanced and metastatic setting. Agreement was moderate to test all men with metastatic castration-resistant PCA, regardless of family history, with stronger agreement to test BRCA1/2 and moderate agreement to test ATM to inform prognosis and targeted therapy. Conclusion To our knowledge, this is the first comprehensive, multidisciplinary consensus statement to address a genetic evaluation framework for inherited PCA in the multigene testing era. Future research should focus on developing a working definition of familial PCA for clinical genetic testing, expanding understanding of genetic contribution to aggressive PCA, exploring clinical use of genetic testing for PCA management, genetic testing of African American males, and addressing the value framework of genetic evaluation and testing men at risk for PCA-a clinically heterogeneous disease.
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- 2018
14. Management of Patients with Advanced Prostate Cancer: The Report of the Advanced Prostate Cancer Consensus Conference APCCC 2017
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Gillessen, Silke, Attard, Gerhardt, Beer, Tomasz M, Beltran, Himisha, Bossi, Alberto, Bristow, Rob, Carver, Brett, Castellano, Daniel, Chung, Byung Ha, Clarke, Noel, Daugaard, Gedske, Davis, Ian D, de Bono, Johann, dos Reis, Rodolfo Borges, Drake, Charles G, Eeles, Ros, Efstathiou, Eleni, Evans, Christopher P, Fanti, Stefano, Feng, Felix, Fizazi, Karim, Frydenberg, Mark, Gleave, Martin, Halabi, Susan, Heidenreich, Axel, Higano, Celestia S, James, Nicolas, Kantoff, Philip, Kellokumpu-Lehtinen, Pirkko-Liisa, Khauli, Raja B, Kramer, Gero, Logothetis, Chris, Maluf, Fernando, Morgans, Alicia K, Morris, Michael J, Mottet, Nicolas, Murthy, Vedang, Oh, William, Ost, Piet, Padhani, Anwar R, Parker, Chris, Pritchard, Colin C, Roach, Mack, Rubin, Mark A, Ryan, Charles, Saad, Fred, Sartor, Oliver, Scher, Howard, Sella, Avishay, Shore, Neal, Smith, Matthew, Soule, Howard, Sternberg, Cora N, Suzuki, Hiroyoshi, Sweeney, Christopher, Sydes, Matthew R, Tannock, Ian, Tombal, Bertrand, Valdagni, Riccardo, Wiegel, Thomas, and Omlin, Aurelius
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Cancer ,Urologic Diseases ,Aging ,Prostate Cancer ,Good Health and Well Being ,Humans ,Male ,Neoplasm Staging ,Practice Guidelines as Topic ,Prostatic Neoplasms ,Advanced and high-risk localized prostate cancer ,Castration-naive and castration-resistant prostate cancer ,Therapeutics ,Consensus ,Oligometastatic prostate cancer ,Clinical Sciences ,Urology & Nephrology - Abstract
BackgroundIn advanced prostate cancer (APC), successful drug development as well as advances in imaging and molecular characterisation have resulted in multiple areas where there is lack of evidence or low level of evidence. The Advanced Prostate Cancer Consensus Conference (APCCC) 2017 addressed some of these topics.ObjectiveTo present the report of APCCC 2017.Design, setting, and participantsTen important areas of controversy in APC management were identified: high-risk localised and locally advanced prostate cancer; "oligometastatic" prostate cancer; castration-naïve and castration-resistant prostate cancer; the role of imaging in APC; osteoclast-targeted therapy; molecular characterisation of blood and tissue; genetic counselling/testing; side effects of systemic treatment(s); global access to prostate cancer drugs. A panel of 60 international prostate cancer experts developed the program and the consensus questions.Outcome measurements and statistical analysisThe panel voted publicly but anonymously on 150 predefined questions, which have been developed following a modified Delphi process.Results and limitationsVoting is based on panellist opinion, and thus is not based on a standard literature review or meta-analysis. The outcomes of the voting had varying degrees of support, as reflected in the wording of this article, as well as in the detailed voting results recorded in Supplementary data.ConclusionsThe presented expert voting results can be used for support in areas of management of men with APC where there is no high-level evidence, but individualised treatment decisions should as always be based on all of the data available, including disease extent and location, prior therapies regardless of type, host factors including comorbidities, as well as patient preferences, current and emerging evidence, and logistical and economic constraints. Inclusion of men with APC in clinical trials should be strongly encouraged. Importantly, APCCC 2017 again identified important areas in need of trials specifically designed to address them.Patient summaryThe second Advanced Prostate Cancer Consensus Conference APCCC 2017 did provide a forum for discussion and debates on current treatment options for men with advanced prostate cancer. The aim of the conference is to bring the expertise of world experts to care givers around the world who see less patients with prostate cancer. The conference concluded with a discussion and voting of the expert panel on predefined consensus questions, targeting areas of primary clinical relevance. The results of these expert opinion votes are embedded in the clinical context of current treatment of men with advanced prostate cancer and provide a practical guide to clinicians to assist in the discussions with men with prostate cancer as part of a shared and multidisciplinary decision-making process.
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- 2018
15. FIGURE 1 from Pain and Its Association with Survival for Black and White Individuals with Advanced Prostate Cancer in the United States
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Rencsok, Emily M., primary, Slopen, Natalie, primary, McManus, Hannah D., primary, Autio, Karen A., primary, Morgans, Alicia K., primary, McSwain, Lawrence, primary, Barata, Pedro, primary, Cheng, Heather H., primary, Dreicer, Robert, primary, Gerke, Travis, primary, Green, Rebecca, primary, Heath, Elisabeth I., primary, Howard, Lauren E., primary, McKay, Rana R., primary, Nowak, Joel, primary, Pileggi, Shannon, primary, Pomerantz, Mark M., primary, Rathkopf, Dana E., primary, Tagawa, Scott T., primary, Whang, Young E., primary, Ragin, Camille, primary, Odedina, Folakemi T., primary, Kantoff, Philip W., primary, Vinson, Jake, primary, Villanti, Paul, primary, Haneuse, Sebastien, primary, Mucci, Lorelei A., primary, and George, Daniel J., primary
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- 2024
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16. Data from Pain and Its Association with Survival for Black and White Individuals with Advanced Prostate Cancer in the United States
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Rencsok, Emily M., primary, Slopen, Natalie, primary, McManus, Hannah D., primary, Autio, Karen A., primary, Morgans, Alicia K., primary, McSwain, Lawrence, primary, Barata, Pedro, primary, Cheng, Heather H., primary, Dreicer, Robert, primary, Gerke, Travis, primary, Green, Rebecca, primary, Heath, Elisabeth I., primary, Howard, Lauren E., primary, McKay, Rana R., primary, Nowak, Joel, primary, Pileggi, Shannon, primary, Pomerantz, Mark M., primary, Rathkopf, Dana E., primary, Tagawa, Scott T., primary, Whang, Young E., primary, Ragin, Camille, primary, Odedina, Folakemi T., primary, Kantoff, Philip W., primary, Vinson, Jake, primary, Villanti, Paul, primary, Haneuse, Sebastien, primary, Mucci, Lorelei A., primary, and George, Daniel J., primary
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- 2024
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17. ArCH: improving the performance of clonal hematopoiesis variant calling and interpretation
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Chan, Irenaeus C C, primary, Panchot, Alex, additional, Schmidt, Evelyn, additional, McNulty, Samantha, additional, Wiley, Brian J, additional, Liu, Jie, additional, Turner, Kimberly, additional, Moukarzel, Lea, additional, Wong, Wendy S W, additional, Tran, Duc, additional, Beeler, J Scott, additional, Batchi-Bouyou, Armel Landry, additional, Machiela, Mitchell J, additional, Karyadi, Danielle M, additional, Krajacich, Benjamin J, additional, Zhao, Junhua, additional, Kruglyak, Semyon, additional, Lajoie, Bryan, additional, Levy, Shawn, additional, Patel, Minal, additional, Kantoff, Philip W, additional, Mason, Christopher E, additional, Link, Daniel C, additional, Druley, Todd E, additional, Stopsack, Konrad H, additional, and Bolton, Kelly L, additional
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- 2024
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18. Data from Marital Status, Living Arrangement, and Survival among Individuals with Advanced Prostate Cancer in the International Registry for Men with Advanced Prostate Cancer
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Chen, Naiyu, primary, McGrath, Colleen B., primary, Ericsson, Caroline I., primary, Vaselkiv, Jane B., primary, Rencsok, Emily M., primary, Stopsack, Konrad H., primary, Guard, Hannah E., primary, Autio, Karen A., primary, Rathkopf, Dana E., primary, Enting, Deborah, primary, Bitting, Rhonda L., primary, Mateo, Joaquin, primary, Githiaka, Charles W., primary, Chi, Kim N., primary, Cheng, Heather H., primary, Davis, Ian D., primary, Anderson, Simon G., primary, Badal, Simone Ann Marie, primary, Bjartell, Anders, primary, Russnes, Kjell M., primary, Heath, Elisabeth I., primary, Pomerantz, Mark M., primary, Henegan, John C., primary, Hyslop, Terry, primary, Esteban, Emilio, primary, Omlin, Aurelius, primary, McDermott, Ray, primary, Fay, Andre P., primary, Popoola, Ademola Alabi, primary, Ragin, Camille, primary, Nowak, Joel, primary, Gerke, Travis, primary, Kantoff, Philip W., primary, George, Daniel J., primary, Penney, Kathryn L., primary, and Mucci, Lorelei A., primary
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- 2024
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19. Supplementary Table 1. from Marital Status, Living Arrangement, and Survival among Individuals with Advanced Prostate Cancer in the International Registry for Men with Advanced Prostate Cancer
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Chen, Naiyu, primary, McGrath, Colleen B., primary, Ericsson, Caroline I., primary, Vaselkiv, Jane B., primary, Rencsok, Emily M., primary, Stopsack, Konrad H., primary, Guard, Hannah E., primary, Autio, Karen A., primary, Rathkopf, Dana E., primary, Enting, Deborah, primary, Bitting, Rhonda L., primary, Mateo, Joaquin, primary, Githiaka, Charles W., primary, Chi, Kim N., primary, Cheng, Heather H., primary, Davis, Ian D., primary, Anderson, Simon G., primary, Badal, Simone Ann Marie, primary, Bjartell, Anders, primary, Russnes, Kjell M., primary, Heath, Elisabeth I., primary, Pomerantz, Mark M., primary, Henegan, John C., primary, Hyslop, Terry, primary, Esteban, Emilio, primary, Omlin, Aurelius, primary, McDermott, Ray, primary, Fay, Andre P., primary, Popoola, Ademola Alabi, primary, Ragin, Camille, primary, Nowak, Joel, primary, Gerke, Travis, primary, Kantoff, Philip W., primary, George, Daniel J., primary, Penney, Kathryn L., primary, and Mucci, Lorelei A., primary
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- 2024
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20. Novel genomic signature predictive of response to immune checkpoint blockade: A pan-cancer analysis from project Genomics Evidence Neo-plasia Information Exchange (GENIE)
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Swami, Nishwant, Hwang, William L., Guo, Jimmy A., Hoffman, Hannah, Abramowitz, Matthew C., Elbakouny, Ziad, Beltran, Himisha, Chipidza, Fallon, Choueiri, Toni, Pra, Alan Dal, Huang, Franklin, Kaochar, Salma, Kantoff, Philip, Kim, Daniel W., Kishan, Amar U., Kobetz, Erin, Marinac, Catherine, Mucci, Lorelei A., Muralidhar, Vinayak, Pollack, Alan, Sanford, Nina N., Schaeffer, Edward M., Spratt, Daniel E., Zhao, Shuang G., Rebbeck, Timothy R., Nguyen, Paul L., Feng, Felix Y., Mahal, Brandon A., and Alshalalfa, Mohammed
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- 2021
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21. Metastasis-Free Survival Is a Strong Surrogate of Overall Survival in Localized Prostate Cancer
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Xie, Wanling, Regan, Meredith M, Buyse, Marc, Halabi, Susan, Kantoff, Philip W, Sartor, Oliver, Soule, Howard, Clarke, Noel W, Collette, Laurence, Dignam, James J, Fizazi, Karim, Paruleker, Wendy R, Sandler, Howard M, Sydes, Matthew R, Tombal, Bertrand, Williams, Scott G, Sweeney, Christopher J, and Group, on behalf of the ICECaP Working
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Biomedical and Clinical Sciences ,Clinical Sciences ,Oncology and Carcinogenesis ,Aging ,Clinical Trials and Supportive Activities ,Prostate Cancer ,Clinical Research ,Prevention ,Urologic Diseases ,Cancer ,Combined Modality Therapy ,Disease-Free Survival ,Endpoint Determination ,Humans ,Male ,Neoplasm Metastasis ,Prostatic Neoplasms ,Randomized Controlled Trials as Topic ,Risk Factors ,Survival Analysis ,ICECaP Working Group ,Oncology & Carcinogenesis ,Oncology and carcinogenesis - Abstract
Purpose Adjuvant therapy for intermediate-risk and high-risk localized prostate cancer decreases the number of deaths from this disease. Surrogates for overall survival (OS) could expedite the evaluation of new adjuvant therapies. Methods By June 2013, 102 completed or ongoing randomized trials were identified and individual patient data were collected from 28 trials with 28,905 patients. Disease-free survival (DFS) and metastasis-free survival (MFS) were determined for 21,140 patients from 24 trials and 12,712 patients from 19 trials, respectively. We evaluated the surrogacy of DFS and MFS for OS by using a two-stage meta-analytic validation model by determining the correlation of an intermediate clinical end point with OS and the correlation of treatment effects on both the intermediate clinical end point and OS. Results Trials enrolled patients from 1987 to 2011. After a median follow-up of 10 years, 45% of 21,140 men and 45% of 12,712 men experienced a DFS and MFS event, respectively. For DFS and MFS, 61% and 90% of the patients, respectively, were from radiation trials, and 63% and 66%, respectively, had high-risk disease. At the patient level, Kendall's τ correlation with OS was 0.85 and 0.91 for DFS and MFS, respectively. At the trial level, R2 was 0.86 (95% CI, 0.78 to 0.90) and 0.83 (95% CI, 0.71 to 0.88) from weighted linear regression of 8-year OS rates versus 5-year DFS and MFS rates, respectively. Treatment effects-measured by log hazard ratios-for the surrogates and OS were well correlated ( R2, 0.73 [95% CI, 0.53 to 0.82] for DFS and 0.92 [95% CI, 0.81 to 0.95] for MFS). Conclusion MFS is a strong surrogate for OS for localized prostate cancer that is associated with a significant risk of death from prostate cancer.
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- 2017
22. The Society for Immunotherapy of Cancer consensus statement on immunotherapy for the treatment of prostate carcinoma
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McNeel, Douglas G, Bander, Neil H, Beer, Tomasz M, Drake, Charles G, Fong, Lawrence, Harrelson, Stacey, Kantoff, Philip W, Madan, Ravi A, Oh, William K, Peace, David J, Petrylak, Daniel P, Porterfield, Hank, Sartor, Oliver, Shore, Neal D, Slovin, Susan F, Stein, Mark N, Vieweg, Johannes, and Gulley, James L
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Biomedical and Clinical Sciences ,Clinical Sciences ,Oncology and Carcinogenesis ,Immunology ,Urologic Diseases ,Vaccine Related ,Aging ,Biotechnology ,Prostate Cancer ,Cancer ,Immunization ,5.1 Pharmaceuticals ,Development of treatments and therapeutic interventions ,Guidelines ,Immunotherapy ,Treatment ,Oncology and carcinogenesis - Abstract
Prostate cancer is the most commonly diagnosed malignancy and second leading cause of cancer death among men in the United States. In recent years, several new agents, including cancer immunotherapies, have been approved or are currently being investigated in late-stage clinical trials for the management of advanced prostate cancer. Therefore, the Society for Immunotherapy of Cancer (SITC) convened a multidisciplinary panel, including physicians, nurses, and patient advocates, to develop consensus recommendations for the clinical application of immunotherapy for prostate cancer patients. To do so, a systematic literature search was performed to identify high-impact papers from 2006 until 2014 and was further supplemented with literature provided by the panel. Results from the consensus panel voting and discussion as well as the literature review were used to rate supporting evidence and generate recommendations for the use of immunotherapy in prostate cancer patients. Sipuleucel-T, an autologous dendritic cell vaccine, is the first and currently only immunotherapeutic agent approved for the clinical management of metastatic castrate resistant prostate cancer (mCRPC). The consensus panel utilized this model to discuss immunotherapy in the treatment of prostate cancer, issues related to patient selection, monitoring of patients during and post treatment, and sequence/combination with other anti-cancer treatments. Potential immunotherapies emerging from late-stage clinical trials are also discussed. As immunotherapy evolves as a therapeutic option for the treatment of prostate cancer, these recommendations will be updated accordingly.
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- 2016
23. FIGURE 2 from Pain and Its Association with Survival for Black and White Individuals with Advanced Prostate Cancer in the United States
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Rencsok, Emily M., primary, Slopen, Natalie, primary, McManus, Hannah D., primary, Autio, Karen A., primary, Morgans, Alicia K., primary, McSwain, Lawrence, primary, Barata, Pedro, primary, Cheng, Heather H., primary, Dreicer, Robert, primary, Gerke, Travis, primary, Green, Rebecca, primary, Heath, Elisabeth I., primary, Howard, Lauren E., primary, McKay, Rana R., primary, Nowak, Joel, primary, Pileggi, Shannon, primary, Pomerantz, Mark M., primary, Rathkopf, Dana E., primary, Tagawa, Scott T., primary, Whang, Young E., primary, Ragin, Camille, primary, Odedina, Folakemi T., primary, Kantoff, Philip W., primary, Vinson, Jake, primary, Villanti, Paul, primary, Haneuse, Sebastien, primary, Mucci, Lorelei A., primary, and George, Daniel J., primary
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- 2024
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24. Supplementary Table S4 from Pain and Its Association with Survival for Black and White Individuals with Advanced Prostate Cancer in the United States
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Rencsok, Emily M., primary, Slopen, Natalie, primary, McManus, Hannah D., primary, Autio, Karen A., primary, Morgans, Alicia K., primary, McSwain, Lawrence, primary, Barata, Pedro, primary, Cheng, Heather H., primary, Dreicer, Robert, primary, Gerke, Travis, primary, Green, Rebecca, primary, Heath, Elisabeth I., primary, Howard, Lauren E., primary, McKay, Rana R., primary, Nowak, Joel, primary, Pileggi, Shannon, primary, Pomerantz, Mark M., primary, Rathkopf, Dana E., primary, Tagawa, Scott T., primary, Whang, Young E., primary, Ragin, Camille, primary, Odedina, Folakemi T., primary, Kantoff, Philip W., primary, Vinson, Jake, primary, Villanti, Paul, primary, Haneuse, Sebastien, primary, Mucci, Lorelei A., primary, and George, Daniel J., primary
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- 2024
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25. Supplementary Figure S2 from Pain and Its Association with Survival for Black and White Individuals with Advanced Prostate Cancer in the United States
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Rencsok, Emily M., primary, Slopen, Natalie, primary, McManus, Hannah D., primary, Autio, Karen A., primary, Morgans, Alicia K., primary, McSwain, Lawrence, primary, Barata, Pedro, primary, Cheng, Heather H., primary, Dreicer, Robert, primary, Gerke, Travis, primary, Green, Rebecca, primary, Heath, Elisabeth I., primary, Howard, Lauren E., primary, McKay, Rana R., primary, Nowak, Joel, primary, Pileggi, Shannon, primary, Pomerantz, Mark M., primary, Rathkopf, Dana E., primary, Tagawa, Scott T., primary, Whang, Young E., primary, Ragin, Camille, primary, Odedina, Folakemi T., primary, Kantoff, Philip W., primary, Vinson, Jake, primary, Villanti, Paul, primary, Haneuse, Sebastien, primary, Mucci, Lorelei A., primary, and George, Daniel J., primary
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- 2024
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26. TABLE 1 from Pain and Its Association with Survival for Black and White Individuals with Advanced Prostate Cancer in the United States
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Rencsok, Emily M., primary, Slopen, Natalie, primary, McManus, Hannah D., primary, Autio, Karen A., primary, Morgans, Alicia K., primary, McSwain, Lawrence, primary, Barata, Pedro, primary, Cheng, Heather H., primary, Dreicer, Robert, primary, Gerke, Travis, primary, Green, Rebecca, primary, Heath, Elisabeth I., primary, Howard, Lauren E., primary, McKay, Rana R., primary, Nowak, Joel, primary, Pileggi, Shannon, primary, Pomerantz, Mark M., primary, Rathkopf, Dana E., primary, Tagawa, Scott T., primary, Whang, Young E., primary, Ragin, Camille, primary, Odedina, Folakemi T., primary, Kantoff, Philip W., primary, Vinson, Jake, primary, Villanti, Paul, primary, Haneuse, Sebastien, primary, Mucci, Lorelei A., primary, and George, Daniel J., primary
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- 2024
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27. TABLE 3 from Pain and Its Association with Survival for Black and White Individuals with Advanced Prostate Cancer in the United States
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Rencsok, Emily M., primary, Slopen, Natalie, primary, McManus, Hannah D., primary, Autio, Karen A., primary, Morgans, Alicia K., primary, McSwain, Lawrence, primary, Barata, Pedro, primary, Cheng, Heather H., primary, Dreicer, Robert, primary, Gerke, Travis, primary, Green, Rebecca, primary, Heath, Elisabeth I., primary, Howard, Lauren E., primary, McKay, Rana R., primary, Nowak, Joel, primary, Pileggi, Shannon, primary, Pomerantz, Mark M., primary, Rathkopf, Dana E., primary, Tagawa, Scott T., primary, Whang, Young E., primary, Ragin, Camille, primary, Odedina, Folakemi T., primary, Kantoff, Philip W., primary, Vinson, Jake, primary, Villanti, Paul, primary, Haneuse, Sebastien, primary, Mucci, Lorelei A., primary, and George, Daniel J., primary
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- 2024
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28. TABLE 4 from Pain and Its Association with Survival for Black and White Individuals with Advanced Prostate Cancer in the United States
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Rencsok, Emily M., primary, Slopen, Natalie, primary, McManus, Hannah D., primary, Autio, Karen A., primary, Morgans, Alicia K., primary, McSwain, Lawrence, primary, Barata, Pedro, primary, Cheng, Heather H., primary, Dreicer, Robert, primary, Gerke, Travis, primary, Green, Rebecca, primary, Heath, Elisabeth I., primary, Howard, Lauren E., primary, McKay, Rana R., primary, Nowak, Joel, primary, Pileggi, Shannon, primary, Pomerantz, Mark M., primary, Rathkopf, Dana E., primary, Tagawa, Scott T., primary, Whang, Young E., primary, Ragin, Camille, primary, Odedina, Folakemi T., primary, Kantoff, Philip W., primary, Vinson, Jake, primary, Villanti, Paul, primary, Haneuse, Sebastien, primary, Mucci, Lorelei A., primary, and George, Daniel J., primary
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- 2024
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29. TABLE 2 from Pain and Its Association with Survival for Black and White Individuals with Advanced Prostate Cancer in the United States
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Rencsok, Emily M., primary, Slopen, Natalie, primary, McManus, Hannah D., primary, Autio, Karen A., primary, Morgans, Alicia K., primary, McSwain, Lawrence, primary, Barata, Pedro, primary, Cheng, Heather H., primary, Dreicer, Robert, primary, Gerke, Travis, primary, Green, Rebecca, primary, Heath, Elisabeth I., primary, Howard, Lauren E., primary, McKay, Rana R., primary, Nowak, Joel, primary, Pileggi, Shannon, primary, Pomerantz, Mark M., primary, Rathkopf, Dana E., primary, Tagawa, Scott T., primary, Whang, Young E., primary, Ragin, Camille, primary, Odedina, Folakemi T., primary, Kantoff, Philip W., primary, Vinson, Jake, primary, Villanti, Paul, primary, Haneuse, Sebastien, primary, Mucci, Lorelei A., primary, and George, Daniel J., primary
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- 2024
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30. Marital status, living arrangement, and survival among individuals with advanced prostate cancer in the International Registry for Men with Advanced Prostate Cancer
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Chen, Naiyu, primary, McGrath, Colleen B., additional, Ericsson, Caroline I., additional, Vaselkiv, Jane B., additional, Rencsok, Emily M., additional, Stopsack, Konrad H., additional, Guard, Hannah E., additional, Autio, Karen A., additional, Rathkopf, Dana E., additional, Enting, Deborah, additional, Bitting, Rhonda L., additional, Mateo, Joaquin, additional, Githiaka, Charles Waihenya., additional, Chi, Kim N., additional, Cheng, Heather H., additional, Davis, Ian D., additional, Anderson, Simon G., additional, Badal, Simone Ann Marie., additional, Bjartell, Anders, additional, Russnes, Kjell M., additional, Heath, Elisabeth I., additional, Pomerantz, Mark M., additional, Henegan, John C., additional, Hyslop, Terry, additional, Esteban, Emilio, additional, Omlin, Aurelius, additional, McDermott, Ray, additional, Fay, Andre P., additional, Popoola, Ademola Alabi., additional, Ragin, Camille, additional, Nowak, Joel, additional, Gerke, Travis, additional, Kantoff, Philip W., additional, George, Daniel J., additional, Penney, Kathryn L., additional, and Mucci, Lorelei A., additional
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- 2024
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31. Supplementary Methods S1 from Pain and Its Association with Survival for Black and White Individuals with Advanced Prostate Cancer in the United States
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Rencsok, Emily M., primary, Slopen, Natalie, primary, McManus, Hannah D., primary, Autio, Karen A., primary, Morgans, Alicia K., primary, McSwain, Lawrence, primary, Barata, Pedro, primary, Cheng, Heather H., primary, Dreicer, Robert, primary, Gerke, Travis, primary, Green, Rebecca, primary, Heath, Elisabeth I., primary, Howard, Lauren E., primary, McKay, Rana R., primary, Nowak, Joel, primary, Pileggi, Shannon, primary, Pomerantz, Mark M., primary, Rathkopf, Dana E., primary, Tagawa, Scott T., primary, Whang, Young E., primary, Ragin, Camille, primary, Odedina, Folakemi T., primary, Kantoff, Philip W., primary, Vinson, Jake, primary, Villanti, Paul, primary, Haneuse, Sebastien, primary, Mucci, Lorelei A., primary, and George, Daniel J., primary
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- 2024
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32. Selenium- or Vitamin E–Related Gene Variants, Interaction with Supplementation, and Risk of High-Grade Prostate Cancer in SELECT
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Chan, June M, Darke, Amy K, Penney, Kathryn L, Tangen, Catherine M, Goodman, Phyllis J, Lee, Gwo-Shu Mary, Sun, Tong, Peisch, Sam, Tinianow, Alex M, Rae, James M, Klein, Eric A, Thompson, Ian M, Kantoff, Philip W, and Mucci, Lorelei A
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Biomedical and Clinical Sciences ,Health Sciences ,Clinical Sciences ,Oncology and Carcinogenesis ,Aging ,Complementary and Integrative Health ,Urologic Diseases ,Genetics ,Clinical Trials and Supportive Activities ,Prevention ,Prostate Cancer ,Nutrition ,Cancer ,Patient Safety ,Clinical Research ,3.3 Nutrition and chemoprevention ,Aetiology ,Prevention of disease and conditions ,and promotion of well-being ,2.1 Biological and endogenous factors ,Good Health and Well Being ,Aged ,Biological Transport ,Biomarkers ,Tumor ,Cohort Studies ,Genetic Variation ,Humans ,Male ,Middle Aged ,Neoplasm Grading ,Pharmacogenomic Variants ,Polymorphism ,Single Nucleotide ,Proportional Hazards Models ,Prostatic Neoplasms ,Risk Factors ,Selenium ,Vitamin E ,Medical and Health Sciences ,Epidemiology ,Biomedical and clinical sciences ,Health sciences - Abstract
BackgroundEpidemiologic studies and secondary analyses of randomized trials supported the hypothesis that selenium and vitamin E lower prostate cancer risk. However, the Selenium and Vitamin E Cancer Prevention Trial (SELECT) showed no benefit of either supplement. Genetic variants involved in selenium or vitamin E metabolism or transport may underlie the complex associations of selenium and vitamin E.MethodsWe undertook a case-cohort study of SELECT participants randomized to placebo, selenium, or vitamin E. The subcohort included 1,434 men; our primary outcome was high-grade prostate cancer (N = 278 cases, Gleason 7 or higher cancer). We used weighted Cox regression to examine the association between SNPs and high-grade prostate cancer risk. To assess effect modification, we created interaction terms between randomization arm and genotype and calculated log likelihood statistics.ResultsWe noted statistically significant (P < 0.05) interactions between selenium assignment, SNPs in CAT, SOD2, PRDX6, SOD3, and TXNRD2, and high-grade prostate cancer risk. Statistically significant SNPs that modified the association of vitamin E assignment and high-grade prostate cancer included SEC14L2, SOD1, and TTPA In the placebo arm, several SNPs, hypothesized to interact with supplement assignment and risk of high-grade prostate cancer, were also directly associated with outcome.ConclusionVariants in selenium and vitamin E metabolism/transport genes may influence risk of overall and high-grade prostate cancer, and may modify an individual man's response to vitamin E or selenium supplementation with regards to these risks.ImpactThe effect of selenium or vitamin E supplementation on high-grade prostate cancer risk may vary by genotype. Cancer Epidemiol Biomarkers Prev; 25(7); 1050-8. ©2016 AACR.
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- 2016
33. Association of genetic variations of selenoprotein genes, plasma selenium levels, and prostate cancer aggressiveness at diagnosis
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Xie, Wanling, Yang, Ming, Chan, June, Sun, Tong, Mucci, Lorelei A, Penney, Kathryn L, Lee, Gwo-Shu Mary, and Kantoff, Philip W
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Biomedical and Clinical Sciences ,Clinical Sciences ,Oncology and Carcinogenesis ,Prevention ,Complementary and Integrative Health ,Cancer ,Genetics ,Urologic Diseases ,Aging ,Prostate Cancer ,2.1 Biological and endogenous factors ,Aetiology ,Case-Control Studies ,Genetic Association Studies ,Genetic Predisposition to Disease ,Genotype ,Glutathione Peroxidase ,Humans ,Male ,Middle Aged ,Neoplasm Invasiveness ,Polymorphism ,Single Nucleotide ,Prostatic Neoplasms ,Selenium ,Selenium-Binding Proteins ,Selenoproteins ,Thioredoxin Reductase 1 ,Thioredoxin Reductase 2 ,prostate cancer ,selenium ,selenoproteins ,Paediatrics and Reproductive Medicine ,Oncology & Carcinogenesis ,Clinical sciences ,Oncology and carcinogenesis - Abstract
BackgroundGenetic variations in some of the selenoprotein genes, alone or together with an individual's selenium status, may influence risk or progression of prostate cancer. We investigated the impact of genetic variants of selenoproteins on plasma selenium levels and cancer aggressiveness at diagnosis in men with localized prostate cancer (PCa).MethodsThe study cohort comprised 722 patients seen at Dana-Farber Cancer Institute who had localized/locally advanced PCa (i.e., stage T3 or less, N0, and M0) from 1994 to 2001. Fifty-five tagging single nucleotide polymorphisms (SNPs) from six selenoprotein genes (TXNRD1, TXNRD2, SEP15, GPX3, SELENBP1, and SEPP1) were analyzed. Logistic regression is used to examine associations of genotypes and plasma selenium levels with risk of aggressive disease, defined as D'Amico intermediate/high risk categories. Step down permutation was applied to adjust for multiple comparisons.ResultsThree hundred and forty-eight patients (48%) had aggressive disease at diagnosis. Two SNPs were associated with cancer aggressiveness at diagnosis (unadjusted P = 0.017 and 0.018, respectively). The odds ratio for aggressive disease in patients carrying TXNRD2 rs1005873-AG/GG genotypes or SELENBP1 rs10788804-AG/AA genotypes was 1.54 (95% CI = 1.08, 2.20) and 1.45 (95% CI = 1.07, 1.98), respectively, compared to TXNRD2 rs1005873-AA or SELENBP1 rs10788804-GG carriers. Four SNPs in TXNRD2 (rs1005873, rs13054371, rs3788310, and rs9606174) and the rs230820 in SEPP1 were associated with plasma selenium levels (unadjusted P
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- 2016
34. Development and Optimization of a Subtraction-Normalized Immunocyte Profiling Signature for Prostate Cancer Active Surveillance Risk Stratification
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Van Neste, Leander, primary, Henao, Ricardo, additional, Wojno, Kirk J., additional, Signes, Jorge, additional, DeHart, Jessica, additional, Busta, Angela, additional, Marriott, Elyse, additional, Willing, Marian, additional, Argentini, Andrea, additional, Hurley, Patrick M., additional, Korman, Howard, additional, Hafron, Jason, additional, Putzi, Mathew, additional, Pieczonka, Chris M., additional, Karsh, Lawrence I., additional, Morris, David S., additional, Kassis, Amin I., additional, and Kantoff, Philip W., additional
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- 2023
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35. Genomic correlates of clinical outcome in advanced prostate cancer
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Abida, Wassim, Cyrta, Joanna, Heller, Glenn, Prandi, Davide, Armenia, Joshua, Coleman, Ilsa, Cieslik, Marcin, Benelli, Matteo, Robinson, Dan, Van Allen, Eliezer M., Sboner, Andrea, Fedrizzi, Tarcisio, Mosquera, Juan Miguel, Robinson, Brian D., De Sarkar, Navonil, Kunju, Lakshmi P., Tomlins, Scott, Wu, Yi Mi, Rodrigues, Daniel Nava, Loda, Massimo, Gopalan, Anuradha, Reuter, Victor E., Pritchard, Colin C., Mateo, Joaquin, Bianchini, Diletta, Miranda, Susana, Carreira, Suzanne, Rescigno, Pasquale, Filipenko, Julie, Vinson, Jacob, Montgomery, Robert B., Beltran, Himisha, Heath, Elisabeth I., Scher, Howard I., Kantoff, Philip W., Taplin, Mary-Ellen, Schultz, Nikolaus, deBono, Johann S., Demichelis, Francesca, Nelson, Peter S., Rubin, Mark A., Chinnaiyan, Arul M., and Sawyers, Charles L.
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- 2019
36. Aneuploidy drives lethal progression in prostate cancer
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Stopsack, Konrad H., Whittaker, Charles A., Gerke, Travis A., Loda, Massimo, Kantoff, Philip W., Mucci, Lorelei A., and Amon, Angelika
- Published
- 2019
37. Humoral Immune Response against Nontargeted Tumor Antigens after Treatment with Sipuleucel-T and Its Association with Improved Clinical Outcome
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GuhaThakurta, Debraj, Sheikh, Nadeem A, Fan, Li-Qun, Kandadi, Harini, Meagher, T Craig, Hall, Simon J, Kantoff, Philip W, Higano, Celestia S, Small, Eric J, Gardner, Thomas A, Bailey, Kate, Vu, Tuyen, DeVries, Todd, Whitmore, James B, Frohlich, Mark W, Trager, James B, and Drake, Charles G
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Urologic Diseases ,Clinical Research ,Cancer ,Immunization ,Prostate Cancer ,Aged ,Antigens ,Neoplasm ,Cancer Vaccines ,Humans ,Immunity ,Humoral ,Immunoglobulin G ,Immunotherapy ,Kaplan-Meier Estimate ,Male ,Middle Aged ,Prostate-Specific Antigen ,Prostatic Neoplasms ,Castration-Resistant ,Tissue Extracts ,Oncology and Carcinogenesis ,Oncology & Carcinogenesis - Abstract
PurposeAntitumor activity of cancer immunotherapies may elicit immune responses to nontargeted (secondary) tumor antigens, or antigen spread. We evaluated humoral antigen spread after treatment with sipuleucel-T, an immunotherapy for asymptomatic or minimally symptomatic metastatic castration-resistant prostate cancer (mCRPC), designed to target prostatic acid phosphatase (PAP; primary antigen).Experimental designSerum samples from patients with mCRPC enrolled in the placebo-controlled phase III IMPACT study (evaluable n = 142) were used to assess humoral antigen spread after treatment with sipuleucel-T. Immunoglobulin G (IgG) responses to self-antigens (including tumor antigens) were surveyed using protein microarrays and confirmed using Luminex xMAP. IgG responses were subsequently validated in ProACT (n = 33), an independent phase II study of sipuleucel-T. Association of IgG responses with overall survival (OS) was assessed using multivariate Cox models adjusted for baseline prostate-specific antigen (PSA) and lactate dehydrogenase levels.ResultsIn patients from IMPACT and ProACT, levels of IgG against multiple secondary antigens, including PSA, KLK2/hK2, K-Ras, E-Ras, LGALS8/PCTA-1/galectin-8, and LGALS3/galectin-3, were elevated after treatment with sipuleucel-T (P < 0.01), but not control. IgG responses (≥ 2-fold elevation posttreatment) occurred in ≥ 25% of patients, appeared by 2 weeks after sipuleucel-T treatment, and persisted for up to 6 months. IgG responses to PSA and LGALS3 were associated with improved OS in sipuleucel-T-treated patients from IMPACT (P ≤ 0.05).ConclusionsSipuleucel-T induced humoral antigen spread in patients with mCRPC. IgG responses were associated with improved OS in IMPACT. The methods and results reported may identify pharmacodynamic biomarkers of clinical outcome after sipuleucel-T treatment, and help in clinical assessments of other cancer immunotherapies. See related commentary by Hellstrom and Hellstrom, p. 3581.
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- 2015
38. In Support of a Patient-Driven Initiative and Petition to Lower the High Price of Cancer Drugs.
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Tefferi, Ayalew, Kantarjian, Hagop, Rajkumar, S Vincent, Baker, Lawrence H, Abkowitz, Jan L, Adamson, John W, Advani, Ranjana Hira, Allison, James, Antman, Karen H, Bast, Robert C, Bennett, John M, Benz, Edward J, Berliner, Nancy, Bertino, Joseph, Bhatia, Ravi, Bhatia, Smita, Bhojwani, Deepa, Blanke, Charles D, Bloomfield, Clara D, Bosserman, Linda, Broxmeyer, Hal E, Byrd, John C, Cabanillas, Fernando, Canellos, George Peter, Chabner, Bruce A, Chanan-Khan, Asher, Cheson, Bruce, Clarkson, Bayard, Cohn, Susan L, Colon-Otero, Gerardo, Cortes, Jorge, Coutre, Steven, Cristofanilli, Massimo, Curran, Walter J, Daley, George Q, DeAngelo, Daniel J, Deeg, H Joachim, Einhorn, Lawrence H, Erba, Harry P, Esteva, Francisco J, Estey, Elihu, Fidler, Isaiah J, Foran, James, Forman, Stephen, Freireich, Emil, Fuchs, Charles, George, James N, Gertz, Morie A, Giralt, Sergio, Golomb, Harvey, Greenberg, Peter, Gutterman, Jordan, Handin, Robert I, Hellman, Samuel, Hoff, Paulo Marcelo, Hoffman, Ronald, Hong, Waun Ki, Horowitz, Mary, Hortobagyi, Gabriel N, Hudis, Clifford, Issa, Jean Pierre, Johnson, Bruce Evan, Kantoff, Philip W, Kaushansky, Kenneth, Khayat, David, Khuri, Fadlo R, Kipps, Thomas J, Kripke, Margaret, Kyle, Robert A, Larson, Richard A, Lawrence, Theodore S, Levine, Ross, Link, Michael P, Lippman, Scott M, Lonial, Sagar, Lyman, Gary H, Markman, Maurie, Mendelsohn, John, Meropol, Neal J, Messinger, Yoav, Mulvey, Therese M, O'Brien, Susan, Perez-Soler, Roman, Pollock, Raphael, Prchal, Josef, Press, Oliver, Radich, Jerald, Rai, Kanti, Rosenberg, Saul A, Rowe, Jacob M, Rugo, Hope, Runowicz, Carolyn D, Sandmaier, Brenda M, Saven, Alan, Schafer, Andrew I, Schiffer, Charles, Sekeres, Mikkael A, Silver, Richard T, Siu, Lillian L, and Steensma, David P
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Humans ,Neoplasms ,Antineoplastic Agents ,Patient Advocacy ,Patient Participation ,Drug Costs ,Prescription Fees ,United States ,Medical and Health Sciences - Published
- 2015
39. Radiographic Progression-Free Survival As a Response Biomarker in Metastatic Castration-Resistant Prostate Cancer: COU-AA-302 Results
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Morris, Michael J, Molina, Arturo, Small, Eric J, de Bono, Johann S, Logothetis, Christopher J, Fizazi, Karim, de Souza, Paul, Kantoff, Philip W, Higano, Celestia S, Li, Jinhui, Kheoh, Thian, Larson, Steven M, Matheny, Shannon L, Naini, Vahid, Burzykowski, Tomasz, Griffin, Thomas W, Scher, Howard I, and Ryan, Charles J
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Urologic Diseases ,Clinical Trials and Supportive Activities ,Prostate Cancer ,Cancer ,Clinical Research ,Abiraterone Acetate ,Androstenes ,Antineoplastic Combined Chemotherapy Protocols ,Biomarkers ,Tumor ,Bone Neoplasms ,Disease-Free Survival ,Double-Blind Method ,Humans ,Male ,Neoplasm Metastasis ,Prednisone ,Prostatic Neoplasms ,Castration-Resistant ,Radiography ,Survival Rate ,Treatment Outcome ,Clinical Sciences ,Oncology and Carcinogenesis ,Oncology & Carcinogenesis - Abstract
PurposeProgression-free survival (PFS) in metastatic castration-resistant prostate cancer (mCRPC) trials has been inconsistently defined and poorly associated with overall survival (OS). A reproducible quantitative definition of radiographic PFS (rPFS) was tested for association with a coprimary end point of OS in a randomized trial of abiraterone in patients with mCRPC.Patients and methodsrPFS was defined as ≥ two new lesions on an 8-week bone scan plus two additional lesions on a confirmatory scan, ≥ two new confirmed lesions on any scan ≥ 12 weeks after random assignment, and/or progression in nodes or viscera on cross-sectional imaging, or death. rPFS was assessed by independent review at 15% of deaths and by investigator review at 15% and 40% of deaths. rPFS and OS association was evaluated by Spearman's correlation.ResultsA total of 1,088 patients were randomly assigned to abiraterone plus prednisone or prednisone alone. At first interim analysis, the hazard ratio (HR) by independent review was 0.43 (95% CI, 0.35 to 0.52; P < .001; abiraterone plus prednisone: median rPFS, not estimable; prednisone: median rPFS, 8.3 months). Similar HRs were obtained by investigator review at the first two interim analyses (HR, 0.49; 95% CI, 0.41 to 0.60; P < .001 and HR, 0.53; 95% CI, 0.45 to 0.62; P < .001, respectively), validating the imaging data assay used. Spearman's correlation coefficient between rPFS and OS was 0.72.ConclusionrPFS was highly consistent and highly associated with OS, providing initial prospective evidence on further developing rPFS as an intermediate end point in mCRPC trials.
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- 2015
40. Associations of prostate cancer risk variants with disease aggressiveness: results of the NCI-SPORE Genetics Working Group analysis of 18,343 cases.
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Helfand, Brian T, Roehl, Kimberly A, Cooper, Phillip R, McGuire, Barry B, Fitzgerald, Liesel M, Cancel-Tassin, Geraldine, Cornu, Jean-Nicolas, Bauer, Scott, Van Blarigan, Erin L, Chen, Xin, Duggan, David, Ostrander, Elaine A, Gwo-Shu, Mary, Zhang, Zuo-Feng, Chang, Shen-Chih, Jeong, Somee, Fontham, Elizabeth TH, Smith, Gary, Mohler, James L, Berndt, Sonja I, McDonnell, Shannon K, Kittles, Rick, Rybicki, Benjamin A, Freedman, Matthew, Kantoff, Philip W, Pomerantz, Mark, Breyer, Joan P, Smith, Jeffrey R, Rebbeck, Timothy R, Mercola, Dan, Isaacs, William B, Wiklund, Fredrick, Cussenot, Olivier, Thibodeau, Stephen N, Schaid, Daniel J, Cannon-Albright, Lisa, Cooney, Kathleen A, Chanock, Stephen J, Stanford, Janet L, Chan, June M, Witte, John, Xu, Jianfeng, Bensen, Jeannette T, Taylor, Jack A, and Catalona, William J
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Humans ,Prostatic Neoplasms ,Neoplasm Invasiveness ,Genetic Predisposition to Disease ,Risk Factors ,Cohort Studies ,Polymorphism ,Single Nucleotide ,Adult ,Aged ,Aged ,80 and over ,Middle Aged ,United States ,Male ,National Cancer Institute (U.S.) ,Genetic Association Studies ,Polymorphism ,Single Nucleotide ,and over ,National Cancer Institute ,Urologic Diseases ,Prostate Cancer ,Human Genome ,Genetics ,Cancer ,Prevention ,Aging ,2.1 Biological and endogenous factors ,Genetics & Heredity ,Complementary and Alternative Medicine ,Paediatrics and Reproductive Medicine - Abstract
Genetic studies have identified single nucleotide polymorphisms (SNPs) associated with the risk of prostate cancer (PC). It remains unclear whether such genetic variants are associated with disease aggressiveness. The NCI-SPORE Genetics Working Group retrospectively collected clinicopathologic information and genotype data for 36 SNPs which at the time had been validated to be associated with PC risk from 25,674 cases with PC. Cases were grouped according to race, Gleason score (Gleason ≤ 6, 7, ≥ 8) and aggressiveness (non-aggressive, intermediate, and aggressive disease). Statistical analyses were used to compare the frequency of the SNPs between different disease cohorts. After adjusting for multiple testing, only PC-risk SNP rs2735839 (G) was significantly and inversely associated with aggressive (OR = 0.77; 95 % CI 0.69-0.87) and high-grade disease (OR = 0.77; 95 % CI 0.68-0.86) in European men. Similar associations with aggressive (OR = 0.72; 95 % CI 0.58-0.89) and high-grade disease (OR = 0.69; 95 % CI 0.54-0.87) were documented in African-American subjects. The G allele of rs2735839 was associated with disease aggressiveness even at low PSA levels (
- Published
- 2015
41. A Transient Increase in Eosinophils Is Associated with Prolonged Survival in Men with Metastatic Castration-Resistant Prostate Cancer Who Receive Sipuleucel-T
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McNeel, Douglas G, Gardner, Thomas A, Higano, Celestia S, Kantoff, Philip W, Small, Eric J, Wener, Mark H, Sims, Robert B, DeVries, Todd, Sheikh, Nadeem A, and Dreicer, Robert
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Biomedical and Clinical Sciences ,Clinical Sciences ,Oncology and Carcinogenesis ,Immunology ,Clinical Trials and Supportive Activities ,Cancer ,Clinical Research ,Prostate Cancer ,Urologic Diseases ,Evaluation of treatments and therapeutic interventions ,6.1 Pharmaceuticals ,Adult ,Aged ,Aged ,80 and over ,Blood Proteins ,Bone Neoplasms ,Cancer Vaccines ,Double-Blind Method ,Eosinophils ,Humans ,Kaplan-Meier Estimate ,Leukocyte Count ,Male ,Middle Aged ,Prognosis ,Prostatic Neoplasms ,Castration-Resistant ,Retrospective Studies ,Tissue Extracts ,Treatment Outcome ,Pharmacology and Pharmaceutical Sciences ,Oncology and carcinogenesis - Abstract
Sipuleucel-T is an autologous cellular immunotherapy used to treat asymptomatic or minimally symptomatic metastatic castration-resistant prostate cancer (mCRPC). Traditional short-term indicators of clinical response commonly used with chemotherapy have not correlated with survival in patients treated with sipuleucel-T. This retrospective study aimed to evaluate laboratory parameters as possible early biomarkers associated with clinical benefit following sipuleucel-T treatment. Patients treated with sipuleucel-T from three randomized, controlled, phase III clinical trials in mCRPC were considered: IMPACT (NCT00065442; n = 512), D9901 (NCT00005947; n = 127), and D9902A (NCT01133704; n = 98). Patients from these trials were included in this study if their samples were analyzed by the central laboratory and if data were available from baseline and ≥ 1 posttreatment time point (n = 377). We found that sipuleucel-T treatment was associated with a transient increase in serum eosinophil count at week 6 that resolved by week 14 in 28% of patients (105 of 377). This eosinophil increase correlated with induced immune response, longer prostate cancer-specific survival [HR, 0.713; 95% confidence interval (CI), 0.525-0.970; P = 0.031], and a trend in overall survival (HR, 0.753; 95% CI, 0.563-1.008; P = 0.057). Median serum globulin protein levels also increased transiently, which was associated with antigen-specific antibody responses; however, this finding did not correlate with longer survival. We conclude that transient increases in eosinophils at week 6 may be a useful, objective, short-term indicator of global immune activation and survival benefit with sipuleucel-T in patients with mCRPC. This observation warrants prospective evaluation in future clinical trials.
- Published
- 2014
42. Quantifying Y chromosome loss in primary and metastatic prostate cancer by chromosome painting.
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Rajanala, Sai Harisha, Ghale, Romina, Nandakumar, Subhiksha, Chadalavada, Kalyani, Lee, Gwo-Shu Mary, Stopsack, Konrad H., Chen, Yu, Nanjangud, Gouri J., Chakraborty, Goutam, and Kantoff, Philip W.
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Y chromosome ,CASTRATION-resistant prostate cancer ,PROSTATE cancer ,METASTASIS ,CHROMOSOMES ,NUDITY - Abstract
Somatic Y chromosome loss in hematopoietic cells is associated with higher mortality in men. However, the status of the Y chromosome in cancer tissue is not fully known due to technical limitations, such as difficulties in labelling and sequencing DNA from the Y chromosome. We have developed a system to quantify Y chromosome gain or loss in patient-derived prostate cancer organoids. Using our system, we observed Y chromosome loss in 4 of the 13 (31%) patient-derived metastatic castration-resistant prostate cancer (mCRPC) organoids; interestingly, loss of Yq (long arm of the Y chromosome) was seen in 38% of patient-derived organoids. Additionally, potential associations were observed between mCRPC and Y chromosome nullisomy. The prevalence of Y chromosome loss was similar in primary and metastatic tissue, suggesting that Y chromosome loss is an early event in prostate cancer evolution and may not a result of drug resistance or organoid derivation. This study reports quantification of Y chromosome loss and gain in primary and metastatic prostate cancer tissue and lays the groundwork for further studies investigating the clinical relevance of Y chromosome loss or gain in mCRPC. [ABSTRACT FROM AUTHOR]
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- 2024
- Full Text
- View/download PDF
43. Development and Optimization of a Subtraction-Normalized Immunocyte Profiling Signature for Prostate Cancer Active Surveillance Risk Stratification.
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Van Neste, Leander, Henao, Ricardo, Wojno, Kirk J., Signes, Jorge, DeHart, Jessica, Busta, Angela, Marriott, Elyse, Willing, Marian, Argentini, Andrea, Hurley, Patrick M., Korman, Howard, Hafron, Jason, Putzi, Mathew, Pieczonka, Chris M., Karsh, Lawrence I., Morris, David S., Kassis, Amin I., and Kantoff, Philip W.
- Abstract
Purpose: Less invasive decision support tools are desperately needed to identify occult high-risk disease in men with prostate cancer (PCa) on active surveillance (AS). For a variety of reasons, many men on AS with low- or intermediate-risk disease forgo the necessary repeat surveillance biopsies needed to identify potentially higher-risk PCa. Here, we describe the development of a blood-based immunocyte transcriptomic signature to identify men harboring occult aggressive PCa. We then validate it on a biopsy-positive population with the goal of identifying men who should not be on AS and confirm those men with indolent disease who can safely remain on AS. This model uses subtraction-normalized immunocyte transcriptomic profiles to risk-stratify men with PCa who could be candidates for AS. Materials and Methods: Men were eligible for enrollment in the study if they were determined by their physician to have a risk profile that warranted prostate biopsy. Both training (n = 1017) and validation cohort (n = 1198) populations had blood samples drawn coincident to their prostate biopsy. Purified CD2D and CD14D immune cells were obtained from peripheral blood mononuclear cells, and RNA was extracted and sequenced. To avoid overfitting and unnecessary complexity, a regularized regression model was built on the training cohort to predict PCa aggressiveness based on the National Comprehensive Cancer Network PCa guidelines. This model was then validated on an independent cohort of biopsy-positive men only, using National Comprehensive Cancer Network unfavorable intermediate risk and worse as an aggressiveness outcome, identifying patients who were not appropriate for AS. Results: The best final model for the AS setting was obtained by combining an immunocyte transcriptomic profile based on 2 cell types with PSA density and age, reaching an AUC of 0.73 (95% CI: 0.69-0.77). The model significantly outperforms (P < .001) PSA density as a biomarker, which has an AUC of 0.69 (95% CI: 0.65-0.73). This model yields an individualized patient risk score with 90% negative predictive value and 50% positive predictive value. Conclusions: While further validation in an intended-use cohort is needed, the immunocyte transcriptomic model offers a promising tool for risk stratification of individual patients who are being considered for AS. [ABSTRACT FROM AUTHOR]
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- 2024
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- View/download PDF
44. SLCO1B3 and SLCO2B1 genotypes, androgen deprivation therapy, and prostate cancer outcomes: a prospective cohort study and meta-analysis
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Rajanala, Sai Harisha, primary, Plym, Anna, additional, Vaselkiv, Jane B, additional, Ebot, Ericka M, additional, Matsoukas, Konstantina, additional, Lin, Zhike, additional, Chakraborty, Goutam, additional, Markt, Sarah C, additional, Penney, Kathryn L, additional, Lee, Gwo-Shu M, additional, Mucci, Lorelei A, additional, Kantoff, Philip W, additional, and Stopsack, Konrad H, additional
- Published
- 2023
- Full Text
- View/download PDF
45. Regular aspirin use and gene expression profiles in prostate cancer patients
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Stopsack, Konrad H., Ebot, Ericka M., Downer, Mary K., Gerke, Travis A., Rider, Jennifer R., Kantoff, Philip W., and Mucci, Lorelei A.
- Published
- 2018
46. The IMAAGEN Study: Effect of Abiraterone Acetate and Prednisone on Prostate Specific Antigen and Radiographic Disease Progression in Patients with Nonmetastatic Castration Resistant Prostate Cancer
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Ryan, Charles J., Crawford, E. David, Shore, Neal D., Underwood, Willie, III, Taplin, Mary-Ellen, Londhe, Anil, Francis, Peter St. John, Phillips, Jennifer, McGowan, Tracy, and Kantoff, Philip W.
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- 2018
- Full Text
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47. Clinical Outcomes of First-line Abiraterone Acetate or Enzalutamide for Metastatic Castration-resistant Prostate Cancer After Androgen Deprivation Therapy + Docetaxel or ADT Alone for Metastatic Hormone-sensitive Prostate Cancer
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Francini, Edoardo, Yip, Steven, Ahmed, Shubidito, Li, Haocheng, Ardolino, Luke, Evan, Carolyn P., Kaymakcalan, Marina, Shaw, Grace K., Kantoff, Philip W., Taplin, Mary-Ellen, Alimohamed, Nimira S., Joshua, Anthony M., Heng, Daniel Y.C., and Sweeney, Christopher J.
- Published
- 2018
- Full Text
- View/download PDF
48. Effects of Androgen Deprivation Therapy on Pain Perception, Quality of Life, and Depression in Men With Prostate Cancer
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Gagliano-Jucá, Thiago, Travison, Thomas G., Nguyen, Paul L., Kantoff, Philip W., Taplin, Mary-Ellen, Kibel, Adam S., Manley, Robert, Hally, Kathleen, Bearup, Richelle, Beleva, Yusnie M., Huang, Grace, Edwards, Robert R., and Basaria, Shehzad
- Published
- 2018
- Full Text
- View/download PDF
49. Prognostic Index Model for Progression-Free Survival in Chemotherapy-Naïve Metastatic Castration-Resistant Prostate Cancer Treated With Abiraterone Acetate Plus Prednisone
- Author
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Ryan, Charles J., Kheoh, Thian, Li, Jinhui, Molina, Arturo, De Porre, Peter, Carles, Joan, Efstathiou, Eleni, Kantoff, Philip W., Mulders, Peter F.A., Saad, Fred, and Chi, Kim N.
- Published
- 2018
- Full Text
- View/download PDF
50. The effect of prior androgen synthesis inhibition on outcomes of subsequent therapy with docetaxel in patients with metastatic castrate‐resistant prostate cancer
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Aggarwal, Rahul, Halabi, Susan, Kelly, William Kevin, George, Daniel, Mahoney, John F, Millard, Frederick, Stadler, Walter M, Morris, Michael J, Kantoff, Philip, Monk, J Paul, Carducci, Michael, Small, Eric J, and Oncology, for the Alliance for Clinical Trials in
- Subjects
Prostate Cancer ,Clinical Research ,Urologic Diseases ,Clinical Trials and Supportive Activities ,Cancer ,6.1 Pharmaceuticals ,Evaluation of treatments and therapeutic interventions ,Aged ,Androgen Antagonists ,Antibodies ,Monoclonal ,Humanized ,Antifungal Agents ,Antineoplastic Combined Chemotherapy Protocols ,Bevacizumab ,Bone Neoplasms ,Chemotherapy ,Adjuvant ,Disease Progression ,Docetaxel ,Drug Therapy ,Combination ,Follow-Up Studies ,Humans ,International Agencies ,Ketoconazole ,Liver Neoplasms ,Lung Neoplasms ,Lymphatic Metastasis ,Male ,Middle Aged ,Neoplasm Staging ,Orchiectomy ,Prednisone ,Prognosis ,Prostatic Neoplasms ,Retrospective Studies ,Survival Rate ,Taxoids ,prostatic neoplasms ,chemotherapy ,ketoconazole ,steroid 17-alpha-hydroxylase ,androgen antagonists ,Alliance for Clinical Trials in Oncology ,Oncology and Carcinogenesis ,Public Health and Health Services ,Oncology & Carcinogenesis - Abstract
BackgroundPreliminary data suggest a potential decreased benefit of docetaxel in patients with metastatic, castration-resistant prostate cancer (mCRPC) who previously received abiraterone acetate, a novel androgen synthesis inhibitor (ASI). Cancer and Leukemia Group B (CALGB) trial 90401 (Alliance), a phase 3 trial in patients with mCRPC who received docetaxel-based chemotherapy, offered the opportunity to evaluate effect of prior ketoconazole, an earlier generation ASI, on clinical outcomes after docetaxel.MethodsIn CALGB trial 90401, 1050 men with chemotherapy-naive mCRPC were randomized to receive treatment with docetaxel and prednisone that included either bevacizumab or placebo. In total, 1005 men (96%) had data available regarding prior ketoconazole therapy. The observed effects of prior ketoconazole on overall survival (OS), progression-free survival (PFS), prostate-specific antigen (PSA) decline, and the objective response rate (ORR) were assessed using proportional hazards and Poisson regression methods adjusted for validated prognostic factors and treatment arm.ResultsBaseline characteristics between patients who did (N=277) and did not (N=728) receive prior ketoconazole therapy were similar. There were no statistically significant differences between patients who did and those who did not receive prior ketoconazole therapy with respect to OS (median OS, 21.1 months vs 22.3 months, respectively; stratified log-rank P=.635), PFS (median PFS, 8.1 months vs 8.6 months, respectively; stratified log-rank P=.342), the proportion achieving a decline ≥ 50% in PSA (61% vs 66%, respectively; relative risk, 1.09; adjusted P=.129), or ORR (39% vs 43%, respectively; relative risk, 1.11; adjusted P=.366).ConclusionsAs measured by OS, PFS, PSA, and the ORR, there was no evidence that prior treatment with ketoconazole had an impact on the clinical outcomes of patients with mCRPC who received subsequent docetaxel-based therapy. The current results highlight the need for prospective studies to assess for potential cross-resistance with novel ASIs and to define the optimal sequence of therapy in mCRPC.
- Published
- 2013
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