Institution
Cancer Care Ontario
Government•Toronto, Ontario, Canada•
About: Cancer Care Ontario is a government organization based out in Toronto, Ontario, Canada. It is known for research contribution in the topics: Population & Cancer. The organization has 970 authors who have published 1605 publications receiving 64954 citations.
Topics: Population, Cancer, Breast cancer, Health care, Odds ratio
Papers published on a yearly basis
Papers
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International Agency for Research on Cancer1, Russian Academy2, Nofer Institute of Occupational Medicine3, Charles University in Prague4, Fred Hutchinson Cancer Research Center5, University of Liverpool6, Cancer Care Ontario7, Princess Margaret Cancer Centre8, Women's College, Kolkata9, Norwegian University of Science and Technology10, German Cancer Research Center11, University of Cambridge12, Umeå University13, University of Bremen14, French Institute of Health and Medical Research15, University of Turin16, University of Aberdeen17, University of Padua18, Newcastle University19, University of Glasgow20, Trinity College, Dublin21
TL;DR: The results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets.
Abstract: Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually. To identify genetic factors that modify disease risk, we conducted a genome-wide association study by analysing 317,139 single-nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer (P = 9 x 10(-10)). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls (P = 5 x 10(-20) overall), and it was found to account for 14% (attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits (CHRNA5, CHRNA3 and CHRNB4). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines, and they bind to N'-nitrosonornicotine and potential lung carcinogens. A non-synonymous variant of CHRNA5 that induces an amino acid substitution (D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets.
1,226 citations
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University of London1, International Agency for Research on Cancer2, Canadian Partnership Against Cancer3, Cancer Council Victoria4, Alberta Health Services5, BC Cancer Agency6, Cancer Care Ontario7, National Board of Health8, Karolinska University Hospital9, Uppsala University Hospital10, Karolinska Institutet11, Cardiff University12
TL;DR: In this paper, the first study in a programme to investigate international survival disparities, with the aim of informing health policy to raise standards and reduce inequalities in survival, was presented, where data from population-based cancer registries in 12 jurisdictions in six countries were provided for 2·4 million adults diagnosed with primary colorectal, lung, breast, ovarian, or ovarian cancer during 1995-2007, with follow-up to Dec 31, 2007.
1,031 citations
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Icahn School of Medicine at Mount Sinai1, Centre national de la recherche scientifique2, French Institute of Health and Medical Research3, Pierre-and-Marie-Curie University4, University of Toronto5, Trinity College, Dublin6, University of Pittsburgh7, Utrecht University8, McMaster University9, Our Lady's Children's Hospital10, University College Dublin11, University of Oxford12, University of Lisbon13, Instituto Nacional de Saúde Dr. Ricardo Jorge14, University of California, Los Angeles15, University of Miami16, Goethe University Frankfurt17, University of Pennsylvania18, Vanderbilt University19, Temple University20, University of Bologna21, Cancer Care Ontario22, University of Southern California23, University of Alberta24, University of Birmingham25, Université de Montréal26, Rush University Medical Center27, University of Coimbra28, Kaiser Permanente29, Cornell University30, Newcastle University31, University of Illinois at Chicago32, University of Minnesota33, University of Gothenburg34, Memorial University of Newfoundland35, Duke University36, University of Paris37, Centre for Mental Health38, King's College London39, University of Washington40, Nationwide Children's Hospital41, Indiana University42, Tufts University43, German Cancer Research Center44, University of Utah45, Stanford University46
TL;DR: For example, the authors analyzed 2,446 ASD-affected families and confirmed an excess of genic deletions and duplications in affected versus control groups (1.41-fold, p = 1.0 × 10(-5)) and an increase in affected subjects carrying exonic pathogenic CNVs overlapping known loci associated with dominant or X-linked ASD and intellectual disability.
Abstract: Rare copy-number variation (CNV) is an important source of risk for autism spectrum disorders (ASDs). We analyzed 2,446 ASD-affected families and confirmed an excess of genic deletions and duplications in affected versus control groups (1.41-fold, p = 1.0 × 10(-5)) and an increase in affected subjects carrying exonic pathogenic CNVs overlapping known loci associated with dominant or X-linked ASD and intellectual disability (odds ratio = 12.62, p = 2.7 × 10(-15), ∼3% of ASD subjects). Pathogenic CNVs, often showing variable expressivity, included rare de novo and inherited events at 36 loci, implicating ASD-associated genes (CHD2, HDAC4, and GDI1) previously linked to other neurodevelopmental disorders, as well as other genes such as SETD5, MIR137, and HDAC9. Consistent with hypothesized gender-specific modulators, females with ASD were more likely to have highly penetrant CNVs (p = 0.017) and were also overrepresented among subjects with fragile X syndrome protein targets (p = 0.02). Genes affected by de novo CNVs and/or loss-of-function single-nucleotide variants converged on networks related to neuronal signaling and development, synapse function, and chromatin regulation.
833 citations
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University of Ottawa1, University of Ioannina2, University of Bern3, Centers for Disease Control and Prevention4, PLOS5, University of Bristol6, Ottawa Hospital Research Institute7, University of Texas Health Science Center at Houston8, University of Western Ontario9, Erasmus University Rotterdam10, Cancer Care Ontario11, McGill University12, Harvard University13
TL;DR: The STREGA recommendations are presented, which are aimed at improving the reporting of genetic association studies and are designed to improve the quality of studies.
Abstract: Making sense of rapidly evolving evidence on genetic associations is crucial to making genuine advances in human genomics and the eventual integration of this information in the practice of medicine and public health. Assessment of the strengths and weaknesses of this evidence, and hence the ability to synthesize it, has been limited by inadequate reporting of results. The STrengthening the REporting of Genetic Association studies (STREGA) initiative builds on the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) Statement and provides additions to 12 of the 22 items on the STROBE checklist. The additions concern population stratification, genotyping errors, modelling haplotype variation, Hardy-Weinberg equilibrium, replication, selection of participants, rationale for choice of genes and variants, treatment effects in studying quantitative traits, statistical methods, relatedness, reporting of descriptive and outcome data, and the volume of data issues that are important to consider in genetic association studies. The STREGA recommendations do not prescribe or dictate how a genetic association study should be designed but seek to enhance the transparency of its reporting, regardless of choices made during design, conduct, or analysis.
766 citations
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TL;DR: Using a multistage genetic association approach comprising 7,480 affected individuals and 7,779 controls, markers in chromosomal region 8q24 associated with colorectal cancer were identified and this locus has been implicated in prostate cancer.
Abstract: Using a multistage genetic association approach comprising 7,480 affected individuals and 7,779 controls, we identified markers in chromosomal region 8q24 associated with colorectal cancer. In stage 1, we genotyped 99,632 SNPs in 1,257 affected individuals and 1,336 controls from Ontario. In stages 2-4, we performed serial replication studies using 4,024 affected individuals and 4,042 controls from Seattle, Newfoundland and Scotland. We identified one locus on chromosome 8q24 and another on 9p24 having combined odds ratios (OR) for stages 1-4 of 1.18 (trend; P = 1.41 x 10(-8)) and 1.14 (trend; P = 1.32 x 10(-5)), respectively. Additional analyses in 2,199 affected individuals and 2,401 controls from France and Europe supported the association at the 8q24 locus (OR = 1.16, trend; 95% confidence interval (c.i.): 1.07-1.26; P = 5.05 x 10(-4)). A summary across all seven studies at the 8q24 locus was highly significant (OR = 1.17, c.i.: 1.12-1.23; P = 3.16 x 10(-11)). This locus has also been implicated in prostate cancer.
739 citations
Authors
Showing all 971 results
Name | H-index | Papers | Citations |
---|---|---|---|
Mark Levine | 115 | 567 | 55828 |
Thomas J. Hudson | 105 | 355 | 68459 |
Steven Gallinger | 99 | 502 | 48181 |
Kathleen I. Pritchard | 96 | 534 | 55670 |
Irene L. Andrulis | 95 | 425 | 33512 |
Bruce K. Armstrong | 89 | 532 | 32270 |
George Tomlinson | 87 | 537 | 31577 |
Jeremy A. Squire | 87 | 344 | 38764 |
Joseph Beyene | 84 | 398 | 25944 |
Michael Sharpe | 84 | 417 | 30546 |
Timothy J. Whelan | 79 | 292 | 35977 |
Brian W. Pogue | 78 | 822 | 24327 |
Mark P. Purdue | 73 | 372 | 19823 |
Padraig Warde | 70 | 420 | 20345 |
Qian Chen | 68 | 599 | 17911 |