Journal article
Genome-Wide Association Studies of Asthma in Population-Based Cohorts Confirm Known and Suggested Loci and Identify an Additional Association near HLA
A Ramasamy, M Kuokkanen, S Vedantam, ZK Gajdos, A Couto Alves, HN Lyon, MAR Ferreira, DP Strachan, JH Zhao, MJ Abramson, MA Brown, L Coin, SC Dharmage, DL Duffy, T Haahtela, AC Heath, C Janson, M Kähönen, KT Khaw, J Laitinen Show all
Plos One | PUBLIC LIBRARY SCIENCE | Published : 2012
Abstract
Rationale: Asthma has substantial morbidity and mortality and a strong genetic component, but identification of genetic risk factors is limited by availability of suitable studies. Objectives: To test if population-based cohorts with self-reported physician-diagnosed asthma and genome-wide association (GWA) data could be used to validate known associations with asthma and identify novel associations. Methods: The APCAT (Analysis in Population-based Cohorts of Asthma Traits) consortium consists of 1,716 individuals with asthma and 16,888 healthy controls from six European-descent population-based cohorts. We examined associations in APCAT of thirteen variants previously reported as genome-wid..
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Awarded by European Commission
Funding Acknowledgements
Please see Supplementary Methods S1 for the details of the many charities, governmental bodies and scientific funding organisations that supported the study recruitment, phenotyping, DNA collection and genotyping for the studies involved in the discovery stage (Stage1) and replication stage (Stage2). The personal research funding supports are listed as follows: AR was supported through the European Commission (through project GABRIEL - contract #018996 under the Integrated Program LSH-2004-1.2.5-1) and the Department of Health, UK. ACA was funded by the European Commission, Framework 7 (grant #223367). The National Health and Medical Research Council, Australia (NHMRC) supported MARF through a project grant (#613627), MAB via a Principal Research Fellowship (#455836) and SCD, DLD, NGM, MCM and GWM via a fellowship scheme. AP acknowledges funding from The Academy of Finland Center of Excellence in Complex Disease Genetics (#213506 and 129680), the Wellcome Trust (#089062), the European Community's Framework 7 Programme and the ENGAGE Consortium (#201413). The Academy of Finland supported EW (#129287, #134839) and VS (#129494, #139635). JE was supported through Academy of Finland, Samfundet Folkhalsan, Finnish Diabetes Research Foundation, Finska Lakaresallskapet, Finnish Foundation for Cardiovascular Research; Yrjo Jahnsson Foundation and Foundation Liv och Halsa. TL was supported by Foundation of the Finnish Anti-Tuberculosis and Allergy Associations. M-RJ has received financial support from the Academy of Finland, Biocenter Oulu, University of Oulu and National Heart Lung and Blood Institute (NHLBI) - National Institutes of Health (#5R01HL087679-02 through the STAMPEED program 1RL1MH083268-01). JNH was supported by a grant from the American Asthma Foundation for analysis of Framingham SHARe data for association with asthma. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.