tbuckley/cabot-search huggingface dataset:
INTEGRATING MYOCARDIAL STRAIN AND EXERCISE PERFORMANCE INTO PROGNOSTICATION OF HYPERTROPHIC CARDIOMYOPATHY
Authors: Kegan Moneghetti, Davide Stolfo, Jeffrey Christle, Yukari Kobayashi, Gherardo Finocchiaro, Gianfranco Sinagra, Jonathan Myers, Euan Ashley, Francois Haddad, Matthew Wheeler
Journal: Journal of the American College of Cardiology (2017)
SAFETY OF SAME DAY DISCHARGE FOLLOWING PCI FOR NON-ST ELEVATION ACUTE CORONARY SYNDROMES
Authors: Ibrahim Kassas, Barinder Hansra, Aditya Vaze, Adedotun Ogunsua, Deeqo Mohamud, Michael Gagnier, Summer Aldrugh, Antoine Soueid, Ahmed Nagy, Jason Stencel, Margaret Oliverio, Kurt Barringhaus, Mohammed Akhter
Journal: Journal of the American College of Cardiology (2017)
Relationship between overall survival and progression-free survival for recent NCCTG glioblastoma multiforme trials.
Authors: Wenting Wu, Evanthia Galanis, Jan C. Buckner, Kurt A. Jaeckle, Daniel J. Sargent
Journal: Journal of Clinical Oncology (2012)

2004 Background: With the approval of novel agents for glioblastoma (GBM) treatment, reliable historical outcome data for the common phase II endpoint of progression free survival (PFS) is not available. In particular, the association between progression and overall survival (OS) has not been evaluated after temozolomide (TMZ) became the standard therapy for newly diagnosed GBM. Methods: Datasets from 5 TMZ-including NCCTG clinical trials in newly diagnosed GBM (n=325, 2005-2011, 1 phase I only and 4 phase I and single arm phase II trials) were pooled and analyzed to evaluate the individual level correlation between PFS and OS using correlation coefficient, landmark analyses, and time-dependent variable analyses. A historical control group was constructed by pooling datasets from 12 pre-TMZ era NCCTG clinical trials in the same patient population (n=1359, 1980-2004). Each of the 5 newer trials was compared to the control group to estimate the treatment effect (hazard ratio) on PFS and OS, which were analyzed to evaluate the trial level correlation between PFS and OS using correlation coefficient and weighted linear regression. Results: The estimated correlation coefficient between PFS and OS at individual patient level is 0.75 (95%CI, 0.7 to 0.8). The estimated hazard ratios of death in the landmark analysis at 4 and 6 months are 2.15 (95%CI, 1.47 to 3.15) and 2.17 (95%CI, 1.57 to 3.12), respectively, and the estimated hazard ratio of death is 10.1 (95%CI, 6.6 to 15.4) when progression is treated as a time-dependent variable. For trial level correlation (against the historical control group), the estimated correlation coefficient between HR os and HR pfs is 0.51 (95%CI, -0.67 to 0.96), with moderate prediction: the predicted HR os is very close to the observed HR os in 4 of 5 cases, however the predicted HR os is significantly different from 1 in only 2 out of 5 cases due to small sample size in other 3 cases. Conclusions: PFS and OS are highly associated at the individual patient level but only moderately at the trial level, the latter possibly due to small sample size in some of the trials. Additional validation in other trials could support use of PFS as a primary endpoint for randomized phase II trials in GBM.
Tolerability and efficacy of a biweekly docetaxel, fluorouracil, leucovorin, oxaliplatin regimen (TFOX) in previously advanced metastatic gastric and oesogastric junction (AGC) adenocarcinoma.
Authors: Simon Pernot, Emmanuel Mitry, Emmanuelle Samalin, Laetitia Dahan, Hajer Turki, Thibault Mazard, Marc Ychou, Jean Francois Seitz, Philippe Rougier, Julien Taïeb
Journal: Journal of Clinical Oncology (2012)

4087 Background: The DCF regimen is superior to 5-FU-Cisplatin in term of response rate (RR) and overall survival (OS) in advanced gastric cancer, but is also more toxic. Oxaliplatin is better tolerated and can effectively replace cisplatin in AGC patients (pts). We hypothesize that incorporating Docetaxel into a simplified FOLFOX regimen should be a tolerable and efficient option, and could facilitate the use of this drug in 1 st line in AGC. Methods: TFOX regimen was given biweekly as follow: Docetaxel (50mg/m2), oxaliplatin (85mg/m2), leucoverin (400mg/m2) and 5FU continuous infusion 48h (2400mg/m2). Main inclusion criteria were: pts with histollogically proven metastatic or locally advanced gastric or oesogastric junction adenocarcinoma, previously untreated, PS≤2. Using Fleming design the primary end point was response rate, needing a sample size of 40 pts. Results: Between 02/2008 and 07/2011, 41 pts with AGC were enrolled (oesogastric junction: 17 pts, diffuse type: 22 pts, metastatic: 37 pts); mean age was 53.5 years (31-73), 26 pts were male. PS 0/1/2: 11/24/6 pts, 14 pts had a relapse after a R0 resection. The total number of cycles administered was 310 (mean 7.6 cycles/pts) and 90% of pts received at least 4 cycles. No toxic death occurred. Grade 3-4 toxicities were observed in 20 pts (48%). Grade 3-4 toxicities were neutropenia (29%) febrile neutropenia (7%), neurotoxicity (10%), asthenia (10%). ORR was 63% (n=26) [IC95% 48-78], with 2 complete responses. Disease control rate (CR+PR+SD) was 78% (n=32) [IC95% 65-90]. Median progression free survival and overall survival were 6.5 months [IC95% 5.02-10.85] and 12.1 months [IC95% 7.25-15.28], respectively. Conclusions: TFOX is effective with a manageable toxicity profile in first line treatment for AGC pts. Tolerability of this regimen compares favourably with DCF reported tolerability. TFOX may be an alternative option for intensive 1 st line treatment and should now be evaluated in randomized trials.
IMPACT OF THE PRESENCE OF CORONARY ARTERY DISEASE AND TIMING OF REVASCULARIZATION ON OUTCOMES OF PATIENTS UNDERGOING TRANS-CATHETER AORTIC VALVE REPLACEMENT: INSIGHTS FROM STS/ACC TVT REGISTRY
Authors: Hambik Tankazyan, Gaurav Tyagi, Amanda Stebbins, Roland Matsouaka, Alice Wang, Sreekanth Vemulapalli, Kenneth Jutzy, Islam Abudayyeh, Wilson Szeto, David Cohen, Vinod Thourani, Anthony Hilliard
Journal: Journal of the American College of Cardiology (2017)
Use of whole genome sequencing to identify novel mutations in distinct subgroups of medulloblastoma.
Authors: Giles W. Robinson, Matthew Parker, Tanya Kranenburg, Charles Lu, Xiang Chen, Li Ding, Timothy Phoenix, Robert Huether, Radhika Thiruvenkatam, Jianmin Wang, John Easton, Arzu Onar-Thomas, Amar J. Gajjar, David W. Ellison, Elaine Mardis, Richard K. Wilson, James Downing, Jinghui Zhang, Richard J. Gilbertson
Journal: Journal of Clinical Oncology (2012)

9518 Background: Medulloblastoma is a malignant childhood brain tumor comprising four discrete subgroups (SHH-subgroup, WNT-subgroup, subgroup-3 and subgroup-4). The genetic alterations that drive these subgroups and that might serve as treatment targets are largely unknown. Methods: We sequenced entire genomes of 37 tumors and matched normal blood. 136 somatically mutated genes identified in this discovery cohort were sequenced in an additional 56 medulloblastomas. All tumors were classified into the 4 subgroups by expression profiling and immunohistochemistry. All mutations were validated by custom capture, 454, or Sanger sequencing. Results: Recurrent mutations were detected in 49 genes: 41 are not yet implicated in medulloblastoma. Several target distinct components of the epigenetic machinery in different disease subgroups, e.g., regulators of H3K27 and H3K4 trimethylation in subgroup-3 and 4 (e.g., KDM6A and ZMYM3), and CTNNB1-associated chromatin remodellers in WNT-subgroup tumors (e.g., SMARCA4 and CREBBP). Modelling of mutations in mouse lower rhombic lip progenitors that generate WNT-subgroup tumours, identified genes that maintain this cell lineage (DDX3X) as well as mutated genes that initiate (CDH1) or cooperate (PIK3CA) in tumourigenesis. Conclusions: We have identified several new recurrent somatic mutations that are enriched in specific subgroups of medulloblastoma. Alterations affecting subgroup-3 and 4 tumors appear to disrupt chromatin marking, most notably H3K27me 3 , potentially preserving a stem cell-like state in tumor cells. Mutations in WNT subgroup tumors affect binding partners of CTNNB1 that regulate WNT-response gene transcription. These data provide important new insights into the pathogenesis of medulloblastoma subgroups and highlight targets for therapeutic development.
Abstract 15417: High Prevalence of Late Onset T in Patients With Long QT Syndrome Type 8
Authors: Seiko Ohno, Junichi Ozawa, Megumi Fukuyama, Takeru Makiyama, Minoru Horie
Journal: Circulation (2016)

Background: In long QT syndrome type 1 to type 3 (LQT3), T wave morphologies (TWMs) in 12-lead-ECGs have been well explored. The consequences of these are helpful to distinguish the genotype before...
Long-term toxicity and survival of definitive chemoradiotherapy (CRT) in patients (pts) with T4/M1LYM esophageal carcinoma
Authors: K. Minashi, A. Ohtsu, K. Mera, S. Yoshida, S. Ishikura, T. Ogino, N. Boku, Y. Miyata, K. Kaneko, A. Nakamura
Journal: Journal of Clinical Oncology (2004)

4209 Background: Although definitive CRT is considered to be standard of care in non-surgical treatment for loco-regional esophageal carcinoma, there have been few reports indicating the treatment results for locally advanced disease. We have previously reported a multicenter phase II trial of the definitive CRT in pts with T4/M1LYM (UICC1987) esophageal carcinoma, which resulted in median survival time of 9months and 3-year survival rate of 23% despite substantial toxicities (Ohtsu et al.JCO'99). The aim of this analysis was to clarify long-term toxicity and survival in pts registered into the study. Methods: Eligibility criteria of this study required T4 and/or M1LYM squamous cell carcinoma of the thoracic esophagus, age ≤ 75, PS 0–2, no prior therapy, and written informed consent. The treatment consisted of 5-FU combined with CDDP and concurrent radiotherapy of 60Gy. For responders, 2 additional courses of chemotherapy were administered. Toxicity and survival data were updated on February 2003, 5.75 years after the last accrual. Late toxicity was evaluated in CR pts using RTOG/EORTC late radiation morbidity scoring schema. Results: From August 1992 to May 1997, 54 pts were enrolled into this trial. There were 36 pts with T4 and 18 with non-T4 (M1LYM only) disease. 18 of 54 pts achieved CR (33%).The updated analysis revealed the actual 5-year survival rate of 17% (9/54): 14% (5/36) in T4 and 22% (4/18) in non-T4 disease. Of the 18 CR pts, grade 3 or worse cardiopulmonary toxicity occurred in 5 (26%) pts: cardiotoxicity in 3 (17%), pleural effusion in 4 (22%), and esophageal stricture in 2 (11%) pts. Eleven of the 18 pts have already died: 7 due to recurrent disease, 3 other malignancies (lung, pancreas, and acute leukemia), and 1 cardiac failure. Seven pts are still alive with no evidence of disease 5.8–8.2 years after initiation of the CRT including 1 pt on-therapy for late toxicity. Conclusions: Definitive CRT provided 17% 5-year survival rate even for unresectable T4/M1LYM esophageal carcinoma, although late toxicity was non-negligible issues that should be addressed. No significant financial relationships to disclose.
Dose Adjusted EPOCH Chemotherapy Plus Rituximab Combination (DA-R-EPOCH), an Effective Upfront Therapy for Patients with Poor-Risk Aggressive B-Cell Lymphomas. Results of a Pilot Study in a Single Center.
Authors: Andrés López, Laura Gallur, Andrés Palacios, Mayda Navarrete, Carmen Ruiz-Marcellán, Josep Castellví, Santiago Ramón y Cajal, Antonio Juliá
Journal: Blood (2005)
Letter by Jin-shan and Xue-bin Regarding Article, “Tachycardia-Induced Cardiomyopathy in a 43-Year-Old Man”
Authors: He Jin-shan, Li Xue-bin
Journal: Circulation (2017)

We read with great interest the wonderful case presented by Zhao et al 1 about dual atrioventricular nodal nonreentrant tachycardia.However, we have several questions.We notice that, aside from the abnormal rhythm, the QRS morphologies in precordial leads are also distorted.The slow and fast pathways conduct the impulse to the ventricle separately, generating 2 different QRS: the former is relatively narrow, the latter wide.However, they are rS or QS in V1 and V2, monomorphic Rs in V5 and V6.This finding indicates a left bundle branch block.Because the left bundle branch refractory period is shorter than the right bundle branch refractory period, it is easier to coincide with the right bundle branch refractory period.This patient's QRS conducted by the slow pathway are all left bundle branch block morphology instead of right bundle branch block, so maybe something is wrong with the left bundle branch.This theory is also proved by the morphology of the QRS conducted by the fast pathway, which are narrow, but present rS in V1 and V2, Rs in V5 and V6.Not all supravenrticular tachycardias cause dilated cardiomyopathy.What is special for this patient?What is the burden of the arrhythmia?Is the left bundle branch block playing a role in this process?Will this patient progress to complete left bundle branch block in the future?I hope long-term follow-up for this patient can answer these questions.
COMPUTED TOMOGRAPHY CORONARY ANGIOGRAPHY DERIVED PLAQUE MORPHOLOGY PREDICTS MAJOR ADVERSE CARDIOVASCULAR EVENTS: INSIGHTS FROM A 19,943 PATIENT META-ANALYSIS
Authors: Nitesh Nerlekar, Caitlin Cheshire, Hashrul Rashid, Rahul Muthalaly, James Cameron, Ian Meredith, Sujith Seneviratne, Dennis Wong, Adam Brown
Journal: Journal of the American College of Cardiology (2017)
INFLUENCE OF LEFT VENTRICULAR EJECTION FRACTION ON CAUSE-SPECIFIC MORTALITY IN HEART FAILURE WITH PRESERVED EJECTION FRACTION: THE TOPCAT TRIAL
Authors: Navkaranbir S. Bajaj, Brian Claggett, Eldrin Lewis, Akshay Desai, James Fang, Eileen Omeara, Sanjiv Shah, Nancy Sweitzer, Jerome Fleg, Bertram Pitt, Jean Rouleau, Peter Finn, Marc Pfeffer, Scott Solomon
Journal: Journal of the American College of Cardiology (2017)
CARDIOLOGIST PERSPECTIVES IN TREATMENT OF DYSLIPIDEMIA PATIENTS WITH PROPROTEIN CONVERTASE SUBTILISIN/KEXIN TYPE 9 INHIBITORS AND OTHER LIPID LOWERING THERAPIES
Authors: Pallavi Rane, Jeetvan Patel, David Harrison, Hollie Bailey, Andrea Leith, James Piercy, Jason Shepherd
Journal: Journal of the American College of Cardiology (2017)
LEFT ATRIAL APPENDAGE OCCLUSION IN PATIENTS WITH ATRIAL FIBRILLATION AND PREVIOUS MAJOR GASTROINTESTINAL BLEEDING: INSIGHT FROM THE AMPLATZER CARDIAC PLUG MULTICENTER REGISTRY
Authors: Mathieu Lempereur, Adel Aminian, Xavier Freixa, Sameer Gafoor, Samera Shakir, Heyder Omran, George Giannakoulas, Sergio Berti, Gennaro Santoro, Joelle Kefer, Ulf Landmesser, Jens Nielsen, Ignacio Cruz-Gonzalez, Prapa Kanagaratnam, Fabian Nietlispach, Reda Ibrahim, Horst Sievert, Wolfgang Schillinger, Jai-Wun Park, Bernhard Meier, Haralampos Karvounis, Apostolos Tzikas
Journal: Journal of the American College of Cardiology (2017)
Eosinophil-derived IL-4 drives progression of myocarditis to inflammatory dilated cardiomyopathy
Authors: Nicola L. Diny, G. Christian Baldeviano, Monica V. Talor, Jobert G. Barin, SuFey Ong, Djahida Bedja, Allison G. Hays, Nisha A. Gilotra, Isabelle Coppens, Noel R. Rose, Daniela Čiháková
Journal: The Journal of Experimental Medicine (2017)

Inflammatory dilated cardiomyopathy (DCMi) is a major cause of heart failure in children and young adults. DCMi develops in up to 30% of myocarditis patients, but the mechanisms involved in disease progression are poorly understood. Patients with eosinophilia frequently develop cardiomyopathies. In this study, we used the experimental autoimmune myocarditis (EAM) model to determine the role of eosinophils in myocarditis and DCMi. Eosinophils were dispensable for myocarditis induction but were required for progression to DCMi. Eosinophil-deficient ΔdblGATA1 mice, in contrast to WT mice, showed no signs of heart failure by echocardiography. Induction of EAM in hypereosinophilic IL-5Tg mice resulted in eosinophilic myocarditis with severe ventricular and atrial inflammation, which progressed to severe DCMi. This was not a direct effect of IL-5, as IL-5TgΔdblGATA1 mice were protected from DCMi, whereas IL-5−/− mice exhibited DCMi comparable with WT mice. Eosinophils drove progression to DCMi through their production of IL-4. Our experiments showed eosinophils were the major IL-4–expressing cell type in the heart during EAM, IL-4−/− mice were protected from DCMi like ΔdblGATA1 mice, and eosinophil-specific IL-4 deletion resulted in improved heart function. In conclusion, eosinophils drive progression of myocarditis to DCMi, cause severe DCMi when present in large numbers, and mediate this process through IL-4.
Result of phase I/IIa multicenter trial for high risk and recurrent neuroblastoma: anti-GD2 antibody (dinutuximab) immunotherapies using M-CSF or G-CSF.
Authors: Hiroshi Kawamoto, Naoko Yasui, Naonori Kawakubo, Chika Nitani, Kenichi Yoshimura, Shigehisa Kitano, Kiyoshi Yoshimura, Toshimi Kimura, Akihiro Sato, Yoji Sasahara, Tomoaki Taguchi, Junichi Hara
Journal: Journal of Clinical Oncology (2015)

e21018 Background: anti-GD2 antibody, dinutuximab (Dmab), with GM-CSF or IL2, has significantly improved outcome in high-risk neuroblastoma (NB) in ANBL0032. Dmab generally induces cell lysis through the process of antibody-dependent Cellular Cytotoxicity (ADCC). To maximize ADCC, this phase I/IIa study was planned to optimize dosing, to confirm feasibility, to evaluate Dmab PK and to evaluate ADCC in using M-CSF (R1) and G-CSF (R2) instead of GM-CSF. Methods: Recurrent NB are eligible and newly diagnosed high-risk NB patients are limited to phase IIa part. In R1, CSF regimen (Dmab 10-20h div d4-7, M-CSF 2h div d1-14) and IL2 regimen (ch14.18 10-20h div d8-11, IL2 24h div d1-4, d8-11) are alternately administered every one month for 5 cycles (up to 7 cycles, if patient (pt) consented), starting from CSF regimen. In R2, G-CSF s.c. is replaced with M-CSF in CSF regimen. Primary endpoint is DLT of Dmab, IL2, M-CSF, G-CSF (phase I (pI)) in 3+3 design and the proportion of completing more than 5 cycles of R1 and R2 (phase IIa (pII)). Results: Sixteen (8 each in R1 and R2) recurrent pts were enrolled. All two DLT (Grade4 thrombocytopenia, Grade3 hypokalemia) of 12 pts in pI occurred only on IL2 regimen (IL2:level0, ch14.18: level1). The recommended dose (RD) of IL2 was level0 (0.75 million IU/m2 (d1-4) and 1 million IU/m2 (d8-11)). the RDs of All the other agents were determined at level1 (Dmab:17.5mg/m2, M-CSF: 6 million IU/m2, G-CSF: 5 ug/kg). SAE were 3 blood stream infections, 1 Grade 3 pancreatitis (inflammation around metastatic lesion in pancreas), 2 upper respiratory infection and 1 Grade4 transaminitis. 7/8 in R1 and 5/8 in R2 completed more than 5 cycles. All eleven consented pts recieved 7 cycles. The result of PK analysis is presented in the following table. Augmentation of ADCC was confirmed in both R1 and R2. More than half pts were positive for HACA assay. Conclusions: R1 and R2 were feasible to be administered repetitively up to 7 courses. Now we are planning a following randomized phase II trial comparing ANBL0032 treatment for selecting better concurrent CSF. Clinical trial information: UMIN000012001. PK parameter AUC 0-inf T1/2beta (h) CL (ml/hr/m2) Vd (L/m2) Dmab 362.8±157.7 76.1±17.0 35.4±14.9 3.9±2.1
IMPORTANT HEMODYNAMIC CONSIDERATIONS IN THE MANAGEMENT OF AN ADULT WITH UNREPAIRED PENTALOGY OF FALLOT PRESENTING WITH NECROTIZING FASCIITIS AND SEPSIS
Authors: Sihong Huang, Daniel Nguyen, Varun Maheshwari, Jasmin Sahbaz, Alexandra Byrne, Geoffrey Rosenthal, Stacy Fisher
Journal: Journal of the American College of Cardiology (2017)
Omega-3 Polyunsaturated Fatty Acid (Fish Oil) Supplementation and the Prevention of Clinical Cardiovascular Disease
Authors: David S. Siscovick, Thomas A. Barringer, Amanda M. Fretts, Jason H.Y. Wu, Alice H. Lichtenstein, Rebecca B. Costello, Penny M. Kris-Etherton, Terry A. Jacobson, Mary B. Engler, Heather M. Alger, Lawrence J. Appel, Dariush Mozaffarian
Journal: Circulation (2017)

Multiple randomized controlled trials (RCTs) have assessed the effects of supplementation with eicosapentaenoic acid plus docosahexaenoic acid (omega-3 polyunsaturated fatty acids, commonly called fish oils) on the occurrence of clinical cardiovascular diseases. Although the effects of supplementation for the primary prevention of clinical cardiovascular events in the general population have not been examined, RCTs have assessed the role of supplementation in secondary prevention among patients with diabetes mellitus and prediabetes, patients at high risk of cardiovascular disease, and those with prevalent coronary heart disease. In this scientific advisory, we take a clinical approach and focus on common indications for omega-3 polyunsaturated fatty acid supplements related to the prevention of clinical cardiovascular events. We limited the scope of our review to large RCTs of supplementation with major clinical cardiovascular disease end points; meta-analyses were considered secondarily. We discuss the features of available RCTs and provide the rationale for our recommendations. We then use existing American Heart Association criteria to assess the strength of the recommendation and the level of evidence. On the basis of our review of the cumulative evidence from RCTs designed to assess the effect of omega-3 polyunsaturated fatty acid supplementation on clinical cardiovascular events, we update prior recommendations for patients with prevalent coronary heart disease, and we offer recommendations, when data are available, for patients with other clinical indications, including patients with diabetes mellitus and prediabetes and those with high risk of cardiovascular disease, stroke, heart failure, and atrial fibrillation.
A randomized phase II clinical trial of enzalutamide in combination with the therapeutic cancer vaccine, PSA tricom, in metastatic, castration resistant prostate cancer.
Authors: Nishith K. Singh, Joseph W. Kim, Christopher Ryan Heery, William L. Dahut, Anna Couvillon, Myrna Rauckhorst, Sheri McMahon, Jeffrey Schlom, Tito Fojo, Philip M. Arlen, James L. Gulley, Ravi Amrit Madan
Journal: Journal of Clinical Oncology (2013)

TPS5104 Background: There is a strong rationale to combine therapeutic cancer vaccines with hormonal abrogation in prostate cancer. Androgen abrogation augments T-cell trafficking to prostate, decreases immune tolerance, increases production of naïve thymic T-cells, enhances cytotoxic T-cell repertoire. PSA TRICOM (PROSTVAC) is a therapeutic, viral-vector based, off-the-shelf, cancer vaccine of PSA &amp; 3 co-stimulatory molecules in phase III testing. This was developed at the NCI in collaboration with Bavarian Nordic Immunotherapeutics. It has demonstrated safety and survival benefit in a randomized phase 2 trial of metastatic castrate resistant prostate cancer (mCRPC). Enzalutamide is a modern androgen receptor inhibitor (ARI) approved for the treatment of mCRPC. Data from the clinical trials with these therapies suggest good individual tolerability without any overlapping toxicities. Analysis of previous trials suggests that vaccines may enhance clinical outcomes with ARI. These data form the scientific basis for a combination approach of a cancer vaccine with ARI to control tumor progression in mCRPC. Methods: A randomized, phase 2, open-label clinical trial at the NCI will enroll 72 chemo-naïve, minimally symptomatic patients with mCRPC. They will be randomized (1:1) to enzalutamide (160 mg daily) alone, or enzalutamide with PSA TRICOM for treatment until radiographic progression. PSA-TRICOM will be administered in a core phase (with day 1, 15 and 29 then 4 additional monthly boosts) followed by continued boosts every 3 months. The primary end point will evaluate time to progression in each arm with secondary endpoints including overall survival and systemic immune responses (lymphocyte subsets, regulatory T-cells, regulatory T-cell function, cytokines, naïve thymic emigrants). If a therapeutic cancer vaccine can enhance the clinical efficacy of a hormonal agent such as enzalutamide, it may help define a new role for vaccines as an adjuvant to standard therapies. We will also evaluate this combination in a second trial in non-metastatic, castration-sensitive patients where this combination may yield its greatest clinical impact.