Institution
University of Calgary
Education•Calgary, Alberta, Canada•
About: University of Calgary is a education organization based out in Calgary, Alberta, Canada. It is known for research contribution in the topics: Population & Health care. The organization has 44284 authors who have published 104970 publications receiving 3669161 citations. The organization is also known as: U of C & UCalgary.
Papers published on a yearly basis
Papers
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TL;DR: The flagship paper of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium describes the generation of the integrative analyses of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types, the structures for international data sharing and standardized analyses, and the main scientific findings from across the consortium studies.
Abstract: Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale1,2,3. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4–5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter4; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation5,6; analyses timings and patterns of tumour evolution7; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity8,9; and evaluates a range of more-specialized features of cancer genomes8,10,11,12,13,14,15,16,17,18.
1,600 citations
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TL;DR: It is suggested that EGF and/or TGF alpha may act on a multipotent progenitor cell in the striatum to generate both neurons and astrocytes.
Abstract: The mitogenic actions of epidermal growth factor (EGF) were examined in low-density, dissociated cultures of embryonic day 14 mouse striatal primordia, under serum-free defined conditions. EGF induced the proliferation of single progenitor cells that began to divide between 5 and 7 d in vitro, and after 13 d in vitro had formed a cluster of undifferentiated cells that expressed nestin, an intermediate filament present in neuroepithelial stem cells. In the continued presence of EGF, cells migrated from the proliferating core and differentiated into neurons and astrocytes. The actions of EGF were mimicked by the homolog transforming growth factor alpha (TGF alpha), but not by NGF, basic fibroblast growth factor, platelet-derived growth factor, or TGF beta. In EGF-generated cultures, cells with neuronal morphology contained immunoreactivity for GABA, substance P, and methionine-enkephalin, three neurotransmitters of the adult striatum. Amplification of embryonic day 14 striatal mRNA by using reverse transcription/PCR revealed mRNAs for EGF, TGF alpha, and the EGF receptor. These findings suggest that EGF and/or TGF alpha may act on a multipotent progenitor cell in the striatum to generate both neurons and astrocytes.
1,598 citations
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TL;DR: Adalimumab was superior to placebo for induction of remission in patients with moderate to severe Crohn's disease naive to anti-TNF therapy and was well tolerated.
1,579 citations
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TL;DR: The epidemiology and pathophysiological mechanisms of cardiovascular risk in patients with chronic kidney disease are discussed, and methods of prevention are discussed.
1,566 citations
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TL;DR: The CD4 cell count at initiation was the dominant prognostic factor in patients starting HAART, and should be taken into account in future treatment guidelines.
1,563 citations
Authors
Showing all 44775 results
Name | H-index | Papers | Citations |
---|---|---|---|
Meir J. Stampfer | 277 | 1414 | 283776 |
Zena Werb | 168 | 473 | 122629 |
William J. Sandborn | 162 | 1317 | 108564 |
Gregg C. Fonarow | 161 | 1676 | 126516 |
David W. Johnson | 160 | 2714 | 140778 |
Jerome I. Rotter | 156 | 1071 | 116296 |
Carl Nathan | 135 | 430 | 91535 |
Severine Vermeire | 134 | 1086 | 76352 |
Ian Ford | 134 | 678 | 85769 |
Jeffery D. Molkentin | 131 | 482 | 61594 |
Joseph P. Broderick | 130 | 504 | 72779 |
Shuai Liu | 129 | 1095 | 80823 |
Marcello Tonelli | 128 | 701 | 115576 |
Gary C. Curhan | 128 | 435 | 55348 |
James C. Paulson | 126 | 443 | 52152 |