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43 results on '"Peterson, Brett J."'

7. Mutations in CHEK2 associated with prostate cancer risk

Author

Dong, Xiangyang, Wang, Liang, Taniguchi, Ken, Wang, Xianshu, Cunningham, Julie M., McDonnell, Shannon K., Qian, Chiping, Marks, Angela F., Slager, Susan L., Peterson, Brett J., Smith, David I., Cheville, John C., Blute, Michael L., Jacobsen, Steve J., Schaid, Daniel J., Tindall, Donald J., Thibodeau, Stephen N., and Liu, Wanguo

Subjects
DNA -- Analysis, Gene mutations -- Analysis, Human genetics -- Research, Prostate cancer -- Risk factors, Prostate cancer -- Genetic aspects, RNA -- Analysis, Biological sciences
Published
2003

8. Analysis of the RNASEL gene in familial and sporadic prostate cancer

Author

Wang, Liang, McDonnell, Shannon K., Elkins, David A., Slager, Susan L., Christensen, Eric, Marks, Angela F., Cunningham, Julie M., Peterson, Brett J., Jacobsen, Steven J., Cerhan, James R., Blute, Michael L., Schaid, Daniel J., and Thibodeau, Stephen N.

Subjects
Gene mutations -- Analysis, Prostate cancer -- Genetic aspects, Genetic polymorphisms -- Analysis, Familial diseases -- Genetic aspects, Biological sciences
Published
2002

20. Characterization of health care utilization in patients receiving implantable cardioverter-defibrillator therapies: An analysis of the managed ventricular pacing trial.

Author

Rickard, John, Whellan, David J., Sherfesee, Lou, Peterson, Brett J., Nahey, Tara, Tang, Anthony S., Ellenbogen, Kenneth A., Cheng, Alan, Rickard, John, Whellan, David J., Sherfesee, Lou, Peterson, Brett J., Nahey, Tara, Tang, Anthony S., Ellenbogen, Kenneth A., and Cheng, Alan

Abstract

BACKGROUND: Implantable cardioverter-defibrillators (ICDs) are effective in terminating lethal arrhythmias, but little is known about the degree of health care utilization (HCU) after ICD therapies. OBJECTIVE: Using data from the managed ventricular pacing trial, we sought to identify the incidence and types of HCU in ICD patients after receiving ICD therapy (shocks or antitachycardia pacing [ATP]). METHODS: We analyzed HCU events (ventricular tachyarrhythmia [VTA]-related, heart failure-related, ICD implant procedure-related, ICD system-related, or other) and their association with ICD therapies (shocked ventricular tachycardia episode, ATP-terminated ventricular tachycardia episode, and inappropriately shocked episode). RESULTS: A total of 1879 HCUs occurred in 695 of 1030 subjects (80% primary prevention) and were classified as follows: 133 (7%) VTA-related, 373 (20%) heart failure-related, 97 (5%) implant procedure-related, 115 (6%) system-related, and 1160 (62%) other. Of 2113 treated VTA episodes, 1680 (80%) received ATP only and 433 (20%) received shocks. Stratifying VTA-related HCUs on the basis of the type of ICD therapy delivered, there were 25 HCUs per 100 shocked VTA episodes compared with 1 HCU per 100 ATP-terminated episodes. Inappropriate ICD shocks occurred in 8.7% of the subjects and were associated with 115 HCUs. The majority of HCUs (52%) began in the emergency department, and 66% of all HCUs resulted in hospitalization. CONCLUSION: For VTA-related HCUs, shocks are associated with a 25-fold increase in HCUs compared to VTAs treated by ATP only. Application of evidence-based strategies and automated device-based algorithms to reduce ICD shocks (higher rate cutoffs, use of ATP, and arrhythmia detection) may help reduce HCUs.

Published
2017

22. Analysis of the Prostate Cancer--Susceptibility Locus HPC20 in 172 Families Affected by Prostate Cancer

Author

Bock, Cathryn H., Cunningham, Julie M., McDonnell, Shannon K., Schaid, Daniel J., Peterson, Brett J., Pavlic, Robert J., Schroeder, Jennifer J., Klein, Jason, French, Amy J., Marks, Angela, Thibodeau, Stephen N., Lange, Ethan M., and Cooney, Kathleen A.

Subjects
Human genetics -- Research, Prostate cancer -- Genetic aspects, Gene mutations -- Research, Biological sciences
Published
2001

23. Evidence for a Prostate Cancer-Susceptibility Locus on Chromosome 20

Author

Berry, Rebecca, Schroeder, Jennifer J., French, Amy J., McDonnell, Shannon K., Peterson, Brett J., Cunningham, Julie M., Thibodeau, Stephen N., and Schaid, Daniel J.

Subjects
Prostate cancer -- Genetic aspects, Human chromosomes -- Research, Disease susceptibility -- Genetic aspects, Biological sciences
Published
2000

24. Linkage Analyses at the Chromosome 1 Loci 1q24-25 (HPC1), 1q42.2-43 (PCAP), and 1p36 (CAPB) in Families with Hereditary Prostate Cancer

Author

Berry, Rebecca, Schaid, Daniel J., Smith, Jeffrey R., French, Amy J., Schroeder, Jennifer J., McDonnell, Shannon K., Peterson, Brett J., Wang, Zheng-Yuan, Carpten, John D., Roberts, Steven G., Tester, David J., Blute, Michael L., Trent, Jeffrey M., and Thibodeau, Stephen N.

Subjects
Linkage (Genetics) -- Analysis, Prostate cancer -- Genetic aspects, Familial diseases -- Analysis, Brain cancer -- Genetic aspects, Biological sciences
Published
2000

27. Lack of current implantable cardioverter defibrillator guidelines application for primary prevention of sudden cardiac death in Latin American patients with heart failure: a cross-sectional study

Author

Gonzalez-Zuelgaray, Jorge, primary, Pellizon, Oscar, additional, Muratore, Claudio A., additional, Oropeza, Elsa Silva, additional, Rabinovich, Rafael, additional, Ramos, José Luis, additional, Tentori, Maria Cristina, additional, Reyes, Nicolás, additional, Aguayo, Rubén, additional, Marin, Jorge, additional, and Peterson, Brett J., additional

Published
2012
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31. Reply

Author

Chow, Theodore, primary and Peterson, Brett J., additional

Published
2009
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39. Does Microvolt T-Wave Alternans Testing Predict Ventricular Tachyarrhythmias in Patients With Ischemic Cardiomyopathy and Prophylactic Defibrillators? The MASTER (Microvolt T Wave Alternans Testing for Risk Stratification of Post-Myocardial Infarction Patients) Trial

Author

Chow, Theodore, Kereiakes, Dean J., Onufer, John, Woelfel, Alan, Gursoy, Sinan, Peterson, Brett J., Brown, Mark L., Pu, Wenji, and Benditt, David G.

Subjects
ventricular arrhythmias, sudden death, T-wave alternans, defibrillator therapy, risk stratification
Abstract

ObjectivesThe purpose of this trial was to determine whether microvolt T-wave alternans (MTWA) predicts ventricular tachyarrhythmic events (VTEs) in post-myocardial infarction patients with left ventricular ejection fraction (LVEF) ≤30%.BackgroundPrevious studies have established MTWA as a predictor for total and arrhythmic mortality, but its ability to identify prophylactic implantable cardioverter-defibrillator (ICD) recipients most likely to experience VTEs remains uncertain.MethodsThis prospective trial was conducted at 50 U.S. centers. Patients were eligible if they met MADIT-II (Multicenter Automatic Defibrillator Implantation Trial II) indications for device implant. All patients underwent MTWA testing followed by ICD implantation, with pre-specified programming to minimize the likelihood of therapies for non–life-threatening VTE. Minimum follow-up was 2 years with annual MTWA testing. Initially indeterminate MTWA tests were repeated.ResultsAnalyses were conducted on 575 patients (84% male; average age ± SD = 65 ± 11 years; average LVEF ± SD = 0.24 ± 0.05). The final distribution of MTWA results were: MTWA positive in 293 (51%), MTWA negative in 214 (37%), and indeterminate in 68 patients (12%). Over an average follow-up of 2.1 ± 0.9 years, there were 70 VTEs. A VTE occurred in 48 of 361 (13%, 6.3%/year) MTWA non-negative and 22 of 214 (10%, 5.0%/year) MTWA negative patients. A non-negative MTWA test result was not associated with VTE (hazard ratio: 1.26; 95% confidence interval: 0.76 to 2.09; p = 0.37), although total mortality was significantly increased (hazard ratio: 2.04; 95% confidence interval: 1.10 to 3.78; p = 0.02).ConclusionsIn MADIT-II–indicated ICD-treated patients, the risk of VTE does not differ according to MTWA classification, despite differences in total mortality. (MASTER I–Microvolt T Wave Alternans Testing for Risk Stratification of Post MI Patients; NCT00305240)

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41. Mutations in CHEK2 Associated with Prostate Cancer Risk.

Author

Xiangyang Dong, Liang Wang, Taniguchi, Ken, Xianshu Wang, Cunningham, Julie M., McDonnell, Shannon K., Chiping Qian, Marks, Angela F., Slager, Susan L., Peterson, Brett J., Smith, David I., Cheville, John C., Blute, Michael L., Jacobsen, Steve J., Schaid, Daniel J., Tindall, Donald J., Thibodeau, Stephen N., and Wanguo Liu

Subjects
*PROSTATE cancer, *CELLULAR signal transduction, *DNA damage
Abstract

The DNA-damage-signaling pathway has been implicated in all human cancers. However, the genetic defects and the mechanisms of this pathway in prostate carcinogenesis remain poorly understood. In this study, we analyzed CHEK2, the upstream regulator of p53 in the DNA-damage-signaling pathway, in several groups of patients with prostate cancer. A total of 28 (4.8%) germline CHEK2 mutations (16 of which were unique) were found among 578 patients. Additional screening for CHEK2 mutations in 149 families with familial prostate cancer revealed 11 mutations (5 unique) in nine families. These mutations included two frameshift and three missense mutations. Importantly, 16 of 18 unique CHEK2 mutations identified in both sporadic and familial cases were not detected among 423 unaffected men, suggesting a pathological effect of CHEK2 mutations in prostate cancer development. Analyses of the two frameshift mutations in Epstein Barr virus-transformed cell lines, using reverse-transcriptase polymerase chain reaction and western blot analysis, revealed abnormal splicing for one mutation and dramatic reduction of CHEK2 protein levels in both cases. Overall, our data suggest that mutations in CHEK2 may contribute to prostate cancer risk and that the DNA-damage-signaling pathway may play an important role in the development of prostate cancer. [ABSTRACT FROM AUTHOR]

Published
2003
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42. Analysis of the RNASEL Gene in Familial and Sporadic Prostate Cancer.

Author

Liang Wang, McDonnell, Shannon K., Elkins, David A., Slager, Susan L., Christensen, Eric, Marks, Angela F., Cunningham, Julie M., Peterson, Brett J., Jacobsen, Steven J., Cerhan, James R., Blute, Michael L., Schaid, Daniel J., and Thibodeau, Stephen N.

Subjects
*HEREDITARY cancer syndromes, *PROSTATE cancer, *FAMILIAL diseases, *GENETICS
Abstract

Presents a study which determined whether the RNASEL gene on chromosome 1q25 is a candidate for hereditary prostrate cancer. Characteristics of the patients; Materials and methods used; Findings and its implications.

Published
2002
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43. Genome linkage screen for prostate cancer susceptibility loci: results from the Mayo Clinic Familial Prostate Cancer Study.

Author

Cunningham JM, McDonnell SK, Marks A, Hebbring S, Anderson SA, Peterson BJ, Slager S, French A, Blute ML, Schaid DJ, and Thibodeau SN

Subjects
Age of Onset, Aged, DNA, Neoplasm chemistry, DNA, Neoplasm genetics, Family, Genetic Markers genetics, Genetic Predisposition to Disease, Humans, Male, Middle Aged, Polymerase Chain Reaction, Sequence Analysis, DNA, Genetic Linkage genetics, Genome, Human, Prostatic Neoplasms genetics
Abstract

Prostate cancer is one of the most common cancers among men and has long been recognized to occur in familial clusters. Brothers and sons of affected men have a twofold to threefold increased risk of developing prostate cancer. However, identification of genetic susceptibility loci for prostate cancer has been extremely difficult. Several putative loci identified by genetic linkage have been reported to exist on chromosomes 1 (HPC1, PCAP, and CAPB), X (HPCX), 17 (HPC2), and 20 (HPC20), with genes RNASEL (HPC1) and ELAC2 (HPC2) tentatively defined. In this study, we report our genome linkage scan in 160 prostate cancer families, using the ABI Prism Linkage Mapping Set Version 2 with 402 microsatellite markers. The most significant linkage was found for chromosome 20, with a recessive model heterogeneity LOD score (HLOD) of 4.77, and a model-free LOD score (LOD - ZLR) of 3.46 for the entire group of pedigrees. Linkage for chromosome 20 was most prominent among families with a late age of diagnosis (average age at diagnosis >/= 66 years; maximum LOD - ZLR = 2.82), with <5 affected family members (LOD - ZLR = 3.02), with presence of hereditary prostate cancer (LOD - ZLR = 2.81), or with no male-to-male transmission of disease (LOD - ZLR = 3.84). No other chromosome showed significant evidence for linkage. However, chromosomes 6 and X showed suggestive results, with maximum LOD - ZLR values of 1.38 and 1.36, respectively. Subset analyses suggest additional chromosomal regions worth further follow-up., (Copyright 2003 Wiley-Liss, Inc.)

Published
2003
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