Lack of Association Between the Trp719Arg Polymorphism in Kinesin-Like Protein-6 and Coronary Artery Disease in 19 Case-Control Studies
Autor: | Thomas M. Morgan, Stephen P. Fortmann, Daniel B. Mirel, Christopher W. Knouff, Willem H. Ouwehand, Sekar Kathiresan, Dawn M. Waterworth, Ingo Ruczinski, Lewis C. Becker, Candace Guiducci, Alan S. Go, Brian G. Kral, Nicola Martinelli, Diane M. Becker, Ron Do, Michael Scholz, Gudmundur Thorgeirsson, Wibke Reinhard, J. Enrique Herrera, Themistocles L. Assimes, Mary Susan Burnett, Liming Qu, Pier Franco Pignatti, Hakon Hakonarson, Rosanna Asselta, Jean Yee, Stefano Duga, Rasika A. Mathias, M Walker, David M. Nathan, Gavin Lucas, Alexander F. Wilson, Roberto Elosua, Richard M. Myers, Martina Grassl, Leena Peltonen, Christa Meisinger, James C. Engert, Stephen E. Epstein, Wolfgang Lieb, Peter S. Braund, H.-Erich Wichmann, Benjamin J. Wright, Patrick Linsel-Nitschke, Mingyao Li, Stefan Schreiber, Klaus Berger, Gordon H. Williams, Alistair S. Hall, Karl Andersen, Jeanette Erdmann, Lisa R. Yanek, Andreas Ziegler, Nauder Faraday, Marcus Fischer, Stephen G. Ball, Yechiel Friedlander, Veikko Salomaa, Stephen M. Schwartz, Bhoom Suktitipat, Joseph M. Devaney, Klaus Stark, Panos Deloukas, Ron Waksman, Changchun Xie, Thomas Scheffold, Michael Preuss, Robert L. Wilensky, François Cambien, Devin Absher, Janina Winogradow, Yoonhee Kim, Andreas Huge, Unnur Thorsteinsdottir, Muredach P. Reilly, Christina Willenborg, Joan Sala, David S. Siscovick, Pascal P. McKeown, Joseph M. Lindsay, Gudmar Thorleifsson, Kenneth M. Kent, Daniel J. Rader, James B. Meigs, Benjamin F. Voight, John R. Thompson, Christopher B. Granger, Elisabetta Trabetti, Vincent Mooser, Stephen Sidney, Neil Risch, Domenico Girelli, Atif Qasim, John A. Spertus, Mark J. Daly, Shaun Purcell, Aki S. Havulinna, David Altshuler, Kari Stefansson, Dhananjay Vaidya, Carlos Iribarren, Christian Hengstenberg, Svati H. Shah, Rafael Ramos, Olle Melander, Mark A. Hlatky, Christopher Patterson, Anthony J. Balmforth, Giovanni Malerba, Calum A. MacRae, Melissa Parkin, William H. Matthai, Christopher J. O'Donnell, Jaume Marrugat, Kiran Musunuru, Monika Stoll, Anika Grosshennig, Augusto D. Pichard, Lowell F. Satler, Hua Tang, Joel N. Hirschhorn, Nilesh J. Samani, Inke R. König, Sandra Eifert, Joshua W. Knowles, Sonia S. Anand, Heribert Schunkert, Thomas Quertermous, Hilma Holm, Isaac Subirana, Oliviero Olivieri |
---|---|
Jazyk: | angličtina |
Předmět: |
Male
medicine.medical_specialty Internationality Kinesins Single-nucleotide polymorphism Genome-wide association study 030204 cardiovascular system & hematology Arginine Polymorphism Single Nucleotide polymorphism Coronary artery disease 03 medical and health sciences 0302 clinical medicine Risk Factors Internal medicine Humans Medicine Prospective cohort study 030304 developmental biology Genetics 0303 health sciences kinesin-like protein 6 KIF6 business.industry Hazard ratio Tryptophan Case-control study Odds ratio Middle Aged medicine.disease myocardial infarction Case-Control Studies coronary artery disease Female Cardiology and Cardiovascular Medicine business Genome-Wide Association Study |
Zdroj: | Assimes, T L, Holm, H, Kathiresan, S, Reilly, M P, Thorleifsson, G, Voight, B F, Erdmann, J, Willenborg, C, Vaidya, D, Xie, C C, Patterson, C, Morgan, T M, Burnett, M S, Li, M Y, Hlatky, M A, Knowles, J W, Thompson, J R, Absher, D, Iribarren, C, Go, A, Fortmann, S P, Sidney, S, Risch, N, Tang, H, Myers, R M, Berger, K, Stoll, M, Shah, S H, Thorgeirsson, G, Andersen, K, Havulinna, A S, Herrera, J E, Faraday, N, Kim, Y, Kral, B G, Mathias, R A, Ruczinski, I, Suktitipat, B, Wilson, A F, Yanek, L R, Becker, L C, Linsel-Nitschke, P, Lieb, W, Konig, I R, Hengstenberg, C, Fischer, M, Stark, K, Reinhard, W, Winogradow, J, Grassl, M, Grosshennig, A, Preuss, M, Schreiber, S, Wichmann, H E, Meisinger, C, Yee, J, Friedlander, Y, Do, R, Meigs, J B, Williams, G, Nathan, D M, MacRae, C A, Qu, L M, Wilensky, R L, Matthai, W H, Qasim, A N, Hakonarson, H, Pichard, A D, Kent, K M, Satler, L, Lindsay, J M, Waksman, R, Knouff, C W, Waterworth, D M, Walker, M C, Mooser, V E, Marrugat, J, Lucas, G, Subirana, I, Sala, J, Ramos, R, Martinelli, N, Olivieri, O, Trabetti, E, Malerba, G, Pignatti, P F, Guiducci, C, Mirel, D, Parkin, M, Hirschhorn, J N, Asselta, R, Duga, S, Musunuru, K, Daly, M J, Purcell, S, Eifert, S, Braund, P S, Wright, B J, Balmforth, A J, Ball, S G, Ouwehand, W H, Deloukas, P, Scholz, M, Cambien, F, Huge, A, Scheffold, T, Salomaa, V, Girelli, D, Granger, C B, Peltonen, L, McKeown, P, Altshuler, D, Melander, O, Devaney, J M, Epstein, S E, Rader, D J, Elosua, R, Engert, J C, Anand, S S, Hall, A S, Ziegler, A, O'Donnell, C J, Spertus, J A, Siscovick, D, Schwartz, S M, Becker, D, Thorsteinsdottir, U, Stefansson, K, Schunkert, H, Samani, N J & Quertermous, T 2010, ' Lack of Association Between the Trp719Arg Polymorphism in Kinesin-Like Protein-6 and Coronary Artery Disease in 19 Case-Control Studies ' Journal of the American College of Cardiology, vol. 56, no. 19, pp. 1552-1563 . DOI: 10.1016/j.jacc.2010.06.022 |
ISSN: | 0735-1097 |
DOI: | 10.1016/j.jacc.2010.06.022 |
Popis: | Objectives We sought to replicate the association between the kinesin-like protein 6 (KIF6) Trp719Arg polymorphism (rs20455), and clinical coronary artery disease (CAD). Background Recent prospective studies suggest that carriers of the 719Arg allele in KIF6 are at increased risk of clinical CAD compared with noncarriers. Methods The KIF6 Trp719Arg polymorphism (rs20455) was genotyped in 19 case-control studies of nonfatal CAD either as part of a genome-wide association study or in a formal attempt to replicate the initial positive reports. Results A total of 17,000 cases and 39,369 controls of European descent as well as a modest number of South Asians, African Americans, Hispanics, East Asians, and admixed cases and controls were successfully genotyped. None of the 19 studies demonstrated an increased risk of CAD in carriers of the 719Arg allele compared with noncarriers. Regression analyses and fixed-effects meta-analyses ruled out with high degree of confidence an increase of >= 2% in the risk of CAD among European 719Arg carriers. We also observed no increase in the risk of CAD among 719Arg carriers in the subset of Europeans with early-onset disease (younger than 50 years of age for men and younger than 60 years of age for women) compared with similarly aged controls as well as all non-European subgroups. Conclusions The KIF6 Trp719Arg polymorphism was not associated with the risk of clinical CAD in this large replication study. (J Am Coll Cardiol 2010;56:1552-63) (C) 2010 by the American College of Cardiology Foundation |
Databáze: | OpenAIRE |
Externí odkaz: |