Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2007-06-07

AUTHORS

Paul R. Burton, David G. Clayton, Lon R. Cardon, Nick Craddock, Panos Deloukas, Audrey Duncanson, Dominic P. Kwiatkowski, Mark I. McCarthy, Willem H. Ouwehand, Nilesh J. Samani, John A. Todd, Peter Donnelly, Jeffrey C. Barrett, Paul R. Burton, Dan Davison, Peter Donnelly, Doug Easton, David Evans, Hin-Tak Leung, Jonathan L. Marchini, Andrew P. Morris, Chris C. A. Spencer, Martin D. Tobin, Lon R. Cardon, David G. Clayton, Antony P. Attwood, James P. Boorman, Barbara Cant, Ursula Everson, Judith M. Hussey, Jennifer D. Jolley, Alexandra S. Knight, Kerstin Koch, Elizabeth Meech, Sarah Nutland, Christopher V. Prowse, Helen E. Stevens, Niall C. Taylor, Graham R. Walters, Neil M. Walker, Nicholas A. Watkins, Thilo Winzer, John A. Todd, Willem H. Ouwehand, Richard W. Jones, Wendy L. McArdle, Susan M. Ring, David P. Strachan, Marcus Pembrey, Gerome Breen, David St Clair, Sian Caesar, Katherine Gordon-Smith, Lisa Jones, Christine Fraser, Elaine K. Green, Detelina Grozeva, Marian L. Hamshere, Peter A. Holmans, Ian R. Jones, George Kirov, Valentina Moskvina, Ivan Nikolov, Michael C. O'Donovan, Michael J. Owen, Nick Craddock, David A. Collier, Amanda Elkin, Anne Farmer, Richard Williamson, Peter McGuffin, Allan H. Young, I. Nicol Ferrier, Stephen G. Ball, Anthony J. Balmforth, Jennifer H. Barrett, D. Timothy Bishop, Mark M. Iles, Azhar Maqbool, Nadira Yuldasheva, Alistair S. Hall, Peter S. Braund, Paul R. Burton, Richard J. Dixon, Massimo Mangino, Suzanne Stevens, Martin D. Tobin, John R. Thompson, Nilesh J. Samani, Francesca Bredin, Mark Tremelling, Miles Parkes, Hazel Drummond, Charles W. Lees, Elaine R. Nimmo, Jack Satsangi, Sheila A. Fisher, Alastair Forbes, Cathryn M. Lewis, Clive M. Onnie, Natalie J. Prescott, Jeremy Sanderson, Christopher G. Mathew, Jamie Barbour, M. Khalid Mohiuddin, Catherine E. Todhunter, John C. Mansfield, Tariq Ahmad, Fraser R. Cummings, Derek P. Jewell, John Webster, Morris J. Brown, David G. Clayton, G. Mark Lathrop, John Connell, Anna Dominiczak, Nilesh J. Samani, Carolina A. Braga Marcano, Beverley Burke, Richard Dobson, Johannie Gungadoo, Kate L. Lee, Patricia B. Munroe, Stephen J. Newhouse, Abiodun Onipinla, Chris Wallace, Mingzhan Xue, Mark Caulfield, Martin Farrall, Anne Barton, The Biologics in RA Genetics and Genomics (BRAGGS), Ian N. Bruce, Hannah Donovan, Steve Eyre, Paul D. Gilbert, Samantha L. Hider, Anne M. Hinks, Sally L. John, Catherine Potter, Alan J. Silman, Deborah P. M. Symmons, Wendy Thomson, Jane Worthington, David G. Clayton, David B. Dunger, Sarah Nutland, Helen E. Stevens, Neil M. Walker, Barry Widmer, John A. Todd, Timothy M. Frayling, Rachel M. Freathy, Hana Lango, John R. B. Perry, Beverley M. Shields, Michael N. Weedon, Andrew T. Hattersley, Graham A. Hitman, Mark Walker, Kate S. Elliott, Christopher J. Groves, Cecilia M. Lindgren, Nigel W. Rayner, Nicholas J. Timpson, Eleftheria Zeggini, Mark I. McCarthy, Melanie Newport, Giorgio Sirugo, Emily Lyons, Fredrik Vannberg, Adrian V. S. Hill, Linda A. Bradbury, Claire Farrar, Jennifer J. Pointon, Paul Wordsworth, Matthew A. Brown, Jayne A. Franklyn, Joanne M. Heward, Matthew J. Simmonds, Stephen C. L. Gough, Sheila Seal, Breast Cancer Susceptibility Collaboration (UK), Michael R. Stratton, Nazneen Rahman, Maria Ban, An Goris, Stephen J. Sawcer, Alastair Compston, David Conway, Muminatou Jallow, Melanie Newport, Giorgio Sirugo, Kirk A. Rockett, Dominic P. Kwiatkowski, Suzannah J. Bumpstead, Amy Chaney, Kate Downes, Mohammed J. R. Ghori, Rhian Gwilliam, Sarah E. Hunt, Michael Inouye, Andrew Keniry, Emma King, Ralph McGinnis, Simon Potter, Rathi Ravindrarajah, Pamela Whittaker, Claire Widden, David Withers, Panos Deloukas, Hin-Tak Leung, Sarah Nutland, Helen E. Stevens, Neil M. Walker, John A. Todd, Doug Easton, David G. Clayton, Paul R. Burton, Martin D. Tobin, Jeffrey C. Barrett, David Evans, Andrew P. Morris, Lon R. Cardon, Niall J. Cardin, Dan Davison, Teresa Ferreira, Joanne Pereira-Gale, Ingileif B. Hallgrimsdóttir, Bryan N. Howie, Jonathan L. Marchini, Chris C. A. Spencer, Zhan Su, Yik Ying Teo, Damjan Vukcevic, Peter Donnelly, David Bentley, Matthew A. Brown, Lon R. Cardon, Mark Caulfield, David G. Clayton, Alistair Compston, Nick Craddock, Panos Deloukas, Peter Donnelly, Martin Farrall, Stephen C. L. Gough, Alistair S. Hall, Andrew T. Hattersley, Adrian V. S. Hill, Dominic P. Kwiatkowski, Christopher G. Mathew, Mark I. McCarthy, Willem H. Ouwehand, Miles Parkes, Marcus Pembrey, Nazneen Rahman, Nilesh J. Samani, Michael R. Stratton, John A. Todd, Jane Worthington

ABSTRACT

There is increasing evidence that genome-wide association (GWA) studies represent a powerful approach to the identification of genes involved in common human diseases. We describe a joint GWA study (using the Affymetrix GeneChip 500K Mapping Array Set) undertaken in the British population, which has examined approximately 2,000 individuals for each of 7 major diseases and a shared set of approximately 3,000 controls. Case-control comparisons identified 24 independent association signals at P < 5 x 10(-7): 1 in bipolar disorder, 1 in coronary artery disease, 9 in Crohn's disease, 3 in rheumatoid arthritis, 7 in type 1 diabetes and 3 in type 2 diabetes. On the basis of prior findings and replication studies thus-far completed, almost all of these signals reflect genuine susceptibility effects. We observed association at many previously identified loci, and found compelling evidence that some loci confer risk for more than one of the diseases studied. Across all diseases, we identified a large number of further signals (including 58 loci with single-point P values between 10(-5) and 5 x 10(-7)) likely to yield additional susceptibility loci. The importance of appropriately large samples was confirmed by the modest effect sizes observed at most loci identified. This study thus represents a thorough validation of the GWA approach. It has also demonstrated that careful use of a shared control group represents a safe and effective approach to GWA analyses of multiple disease phenotypes; has generated a genome-wide genotype database for future studies of common diseases in the British population; and shown that, provided individuals with non-European ancestry are excluded, the extent of population stratification in the British population is generally modest. Our findings offer new avenues for exploring the pathophysiology of these important disorders. We anticipate that our data, results and software, which will be widely available to other investigators, will provide a powerful resource for human genetics research. More... »

PAGES

661

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature05911

    DOI

    http://dx.doi.org/10.1038/nature05911

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1004556449

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/17554300


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