Institution
Emory University
Education•Atlanta, Georgia, United States•
About: Emory University is a education organization based out in Atlanta, Georgia, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 51959 authors who have published 122469 publications receiving 6010698 citations.
Topics: Population, Poison control, Transplantation, Health care, Cancer
Papers published on a yearly basis
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University of Toronto1, German Cancer Research Center2, Harvard University3, Broad Institute4, University of British Columbia5, Heidelberg University6, Memorial Sloan Kettering Cancer Center7, Vanderbilt University8, Sanford-Burnham Institute for Medical Research9, Medical University of Vienna10, Curie Institute11, University of Lausanne12, Seoul National University13, Johns Hopkins University14, University of Lyon15, University of Pittsburgh16, University of Michigan17, University of Alabama at Birmingham18, Catholic University of the Sacred Heart19, Erasmus University Rotterdam20, Boston Children's Hospital21, University of Washington22, Masaryk University23, McMaster University24, Hamilton Health Sciences25, Duke University26, McGill University27, McGill University Health Centre28, Newcastle University29, University of California, San Francisco30, University of Debrecen31, Tohoku University32, Saint Louis University33, Washington University in St. Louis34, University of California, Los Angeles35, Emory University36, University of Cincinnati37, Kumamoto University38, Semmelweis University39, University of Arkansas for Medical Sciences40, University of Naples Federico II41, Chonnam National University42, University of São Paulo43, University of Colorado Denver44, University of Ulsan45, University of Calgary46, Stanford University47
TL;DR: Somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas are reported, including recurrent events targeting TGF-β signalling in Group 3, and NF-κB signalling in Groups 4, which suggest future avenues for rational, targeted therapy.
Abstract: Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4α. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-β signalling in Group 3, and NF-κB signalling in Group 4, suggest future avenues for rational, targeted therapy.
749 citations
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TL;DR: This study represents the most comprehensive definition of transcription factor binding sites in a metazoan species.
748 citations
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TL;DR: The approach to OX-PHOS investigation combines the identification of patients with OX -PHOS defects using more sensitive muscle biopsy studies followed by further biochemical characterization of primary defects in Epstein–Barr virus-transformed lymphoblasts.
Abstract: Publisher Summary This chapter discusses the methods of assessment of mitochondrial oxidative phosphorylation in patient muscle biopsies, lymphoblasts, and transmitochondrial cell lines. Investigation of oxidative phosphorylation (OX-PHOS) in mitochondrial diseases has traditionally focused on the muscle biopsy. Skeletal muscle biopsy remains a valuable resource for biochemical studies as it is an easily accessed tissue and milligram quantities of mitochondria can be isolated for a wide range of OX-PHOS investigations. However, in mitochondrial diseases, the postmitotic muscle fibers commonly show secondary OX-PHOS defects that may hinder investigations of primary defects. Transformed cell lines expressing OX-PHOS defects provide a powerful model system for further genetic and biochemical characterization of nuclear and mitochondrial DNA (mtDNA) mutants and the design and testing of therapeutic approaches. The approach to OX-PHOS investigation combines the identification of patients with OX-PHOS defects using more sensitive muscle biopsy studies followed by further biochemical characterization of primary defects in Epstein–Barr virus-transformed lymphoblasts. The chapter presents novel methods for the production of transmitochondrial cybrids using lymphoblastoid and osteosarcoma ρO cells as recipients. Suspension enucleation of cells combined with electrofusion allows the use of any cell type, including lymphoblasts, as mitochondrial donors in fusions with either lymphoblastoid or osteosarcoma ρo cells.
748 citations
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Duke University1, University of Helsinki2, University of Copenhagen3, University of Nebraska Medical Center4, University of North Carolina at Chapel Hill5, Emory University6, Queen Mary University of London7, Indiana University – Purdue University Indianapolis8, Cleveland Clinic9, University of Hong Kong10, Tufts University11, Tata Memorial Hospital12, Vanderbilt University13, University of Texas MD Anderson Cancer Center14, Columbia University15, Northwestern University16, National Institutes of Health17
TL;DR: An integrative analysis of whole-exome sequencing and transcriptome sequencing in a cohort of DLBCL patients is performed to comprehensively define the landscape of 150 genetic drivers of the disease and their functional roles to identify new therapeutic opportunities in the disease.
747 citations
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TL;DR: The incidence of pneumococcal disease caused by nonvaccine serotypes is increasing and Ongoing surveillance is needed to monitor the magnitude of disease cause by non vaccines, to ensure that future vaccines target the appropriate serotypes.
Abstract: Background. Widespread use of pneumococcal conjugate vaccine (PCV7) resulted in decreases in invasive disease among children and elderly persons. The benefits may be offset by increases in disease due to serotypes not included in the vaccine (hereafter, "nonvaccine serotypes"). We evaluated the effect of PCV7 on incidence of disease due to nonvaccine serotypes. Methods. Cases of invasive disease were identified in 8 geographic areas through the Centers for Disease Control and Prevention's Active Bacterial Core surveillance. Serotyping and susceptibility testing of isolates were performed. We calculated the incidence of disease for children aged <5 years and adults aged ≥65 years. We compared rates of serotype-specific disease before and after PCV7 was licensed for use. Results. The annual incidence of disease due to nonvaccine serotypes increased from an average of 16.3 cases/ 100,000 population during prevaccine years (1998-1999) to 19.9 cases/100,000 population in 2004 for children aged <5 years (P =.01) and from 27.0 cases/100,000 population during prevaccine years to 29.8 cases/100,000 population in 2004 for adults aged ≥65 years (P =.05). Significant increases in the incidences of disease due to serotypes 3, 15, 19A, 22F, and 33F were observed among children during this period (P<.05 for each serotype); serotype 19A has become the predominant cause of invasive disease in children. The incidence of disease due to these serotypes also increased among elderly persons. Conclusions. The incidence of pneumococcal disease caused by nonvaccine serotypes is increasing. Ongoing surveillance is needed to monitor the magnitude of disease caused by nonvaccine serotypes, to ensure that future vaccines target the appropriate serotypes.
747 citations
Authors
Showing all 52622 results
Name | H-index | Papers | Citations |
---|---|---|---|
Younan Xia | 216 | 943 | 175757 |
Eric J. Topol | 193 | 1373 | 151025 |
Bernard Rosner | 190 | 1162 | 147661 |
Paul G. Richardson | 183 | 1533 | 155912 |
Peter W.F. Wilson | 181 | 680 | 139852 |
Dennis S. Charney | 179 | 802 | 122408 |
Joseph Biederman | 179 | 1012 | 117440 |
Kenneth C. Anderson | 178 | 1138 | 126072 |
David A. Weitz | 178 | 1038 | 114182 |
Lei Jiang | 170 | 2244 | 135205 |
William J. Sandborn | 162 | 1317 | 108564 |
Stephen J. Elledge | 162 | 406 | 112878 |
Ali H. Mokdad | 156 | 634 | 160599 |
Michael Tomasello | 155 | 797 | 93361 |
Don W. Cleveland | 152 | 444 | 84737 |