Title: Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls
Authors: Wellcome Trust Case Control Consortium ×
Cardon, Lon R
Craddock, Nick
Deloukas, Panos
Duncanson, Audrey
Kwiatkowski, Dominic P
McCarthy, Mark I
Ouwehand, Willem H
Samani, Nilesh J
Todd, John A
Donnelly, Peter
Barrett, Jeffrey C
Davison, Dan
Easton, Doug
Evans, David
Leung, Hin-Tak
Marchini, Jonathan L
Morris, Andrew P
Spencer, Chris C. A
Tobin, Martin D
Attwood, Antony P
Boorman, James P
Cant, Barbara
Everson, Ursula
Hussey, Judith M
Jolley, Jennifer D
Knight, Alexandra S
Koch, Kerstin
Meech, Elizabeth
Nutland, Sarah
Prowse, Christopher V
Stevens, Helen E
Taylor, Niall C
Walters, Graham R
Walker, Neil M
Watkins, Nicholas A
Winzer, Thilo
Jones, Richard W
McArdle, Wendy L
Ring, Susan M
Strachan, David P
Pembrey, Marcus
Breen, Gerome
St Clair, David
Caesar, Sian
Gordon-Smith, Katherine
Jones, Lisa
Fraser, Christine
Green, Elain K
Grozeva, Detelina
Hamshere, Marian L
Holmans, Peter A
Jones, Ian R
Kirov, George
Moskvina, Valentina
Nikolov, Ivan
O'Donovan, Michael C
Owen, Michael J
Collier, David A
Elkin, Amanda
Farmer, Anne
Williamson, Richard
McGuffin, Peter
Young, Allan H
Ferrier, I. Nicol
Ball, Stephen G
Balmforth, Anthony J
Barrett, Jennifer H
Bishop, D. Timothy
Iles, Mark M
Maqbool, Azhar
Yudasheve, Nadira
Hall, Alistair S
Braund, Peter S
Dixon, Richard J
Mangino, Massimo
Stevens, Suzanne
Thompson, John R
Bredin, Francesca
Tremelling, Mark
Parkes, Miles
Drummond, Hazel
Lees, Charles W
Nimmo, Elaine R
Satsangi, Jack
Fisher, Sheila A
Forbes, Alistair
Lewis, Cathryn M
Onnie, Clive M
Prescott, Natalie J
Sanderson, Jeremy
Mathew, Christopher G
Barbour, Jamie
Mohiuddin, M. Khalid
Todhunter, Catherine E
Mansfield, John C
Ahmad, Tariq
Cummings, Fraser R
Jewell, Derek P
Webster, John
Brown, Morris J
Lathrop, G. Mark
Connell, John
Dominiczak, Anna
Marcano, Carolina A. Braga
Burke, Beverley
Dobson, Richard
Gungadoo, Johannie
Lee, Kate L
Munroe, Patricia B
Newhouse, Stephen J
Onipinla, Abiodun
Wallace, Chris
Xue, Mingzhan
Caulfield, Mark
Farrall, Martin
Barton, Anne
Bruce, Ian N
Donovan, Hannah
Eyre, Steve
Gilbert, Paul D
Hider, Samantha L
Hinks, Anne M
John, Sally L
Potter, Catherine
Silman, Alan J
Symmons, Deborah P. M
Thomson, Wendy
Worthington, Jane
Dunger, David B
Widmer, Barry
Frayling, Timothy M
Freathy, Rachel M
Lango, Hana
Perry, John R. B
Shields, Beverley M
Weedon, Michael N
Hattersley, Andrew T
Elliott, Kate S
Groves, Christopher J
Lindgren, Cecilia M
Rayner, Nigel W
Timpson, Nicholas J
Zeggini, Eleftheria
Newport, Melanie
Sirugo, Giorgio
Lynons, Emily
Vannberg, Fredrik
Brown, Matthew A
Franklyn, Jayne A
Heward, Joanne M,
Simmonds, Matthew J
Hill, Adrian V. S
Bradbury, Linda A
Farrar, Claire
Pointon, Jennifer J
Wordsmith, Paul
Gough, Stephen C. L
Seal, Sheila
Stratton, Michael R
Rahman, Nazneen
Ban, Maria
Goris, An
Sawcer, Stephen J
Compston, Alistair
Conway, David
Jallow, Muminatou
Bumpstead, Suzannah J
Chaney, Amy
Downes, Kate
Ghori, Mohammed J. R
Gwilliam, Rhian
Inouye, Michael
Keniry, Andrew
King, Emma
McGinnis, Ralph
Potter, Simon
Ravindrarajah, Rathi
Whittaker, Pamela
Withers, David
Easton, Doug
Pereira-Gale, Joanne
Hallgrimsdottir, Ingilef B
Howie, Bryan N
Su, Zhan
Teo, Yik Ying
Vukcevic, Damjan
Bentley, David
Caulfield, Mark
Mathew, Christopher G
Worthington, Jane #
Issue Date: Jun-2007
Publisher: Nature publishing group
Series Title: Nature vol:447 issue:7145 pages:661-678
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 similar to 2,000 individuals for each of 7 major diseases and a shared set of similar to 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.
ISSN: 0028-0836
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Research Group Experimental Neurology
Laboratory for Neuroimmunology
× corresponding author
# (joint) last author

Files in This Item:
File Description Status SizeFormat
Nature_WTCCC.pdf Published 4207KbAdobe PDFView/Open Request a copy

These files are only available to some KU Leuven Association staff members


All items in Lirias are protected by copyright, with all rights reserved.

© Web of science