Lack of Association Between the Trp719Arg Polymorphism in Kinesin-Like Protein-6 and Coronary Artery Disease in 19 Case-Control Studies

被引：71

作者：

Assimes, Themistocles L. ^{[1
]}

Holm, Hilma ^{[2
]}

Kathiresan, Sekar ^{[3
,4
,5
,6
,7
]}

Reilly, Muredach P. ^{[8
,9
]}

Thorleifsson, Gudmar ^{[2
]}

Voight, Benjamin F. ^{[5
,6
,10
]}

Erdmann, Jeanette ^{[11
]}

Willenborg, Christina ^{[11
,12
]}

Vaidya, Dhananjay ^{[13
]}

Xie, Changchun ^{[14
,15
,16
]}

Patterson, Chris C. ^{[17
]}

Morgan, Thomas M. ^{[18
]}

Burnett, Mary Susan ^{[19
]}

Li, Mingyao

Hlatky, Mark A. ^{[1
]}

Knowles, Joshua W. ^{[1
]}

Thompson, John R. ^{[20
]}

Absher, Devin ^{[21
]}

Iribarren, Carlos ^{[22
]}

Go, Alan ^{[22
]}

Fortmann, Stephen P. ^{[1
]}

Sidney, Stephen ^{[22
]}

Risch, Neil ^{[23
]}

Tang, Hua ^{[24
]}

Myers, Richard M. ^{[21
]}

Berger, Klaus ^{[25
]}

Stoll, Monika ^{[26
]}

Shah, Svati H. ^{[27
,28
]}

Thorgeirsson, Gudmundur ^{[29
,30
]}

Andersen, Karl ^{[29
,30
]}

Havulinna, Aki S. ^{[31
]}

Herrera, J. Enrique ^{[13
]}

Faraday, Nauder ^{[32
]}

Kim, Yoonhee ^{[33
]}

Kral, Brian G. ^{[13
]}

Mathias, Rasika A. ^{[13
]}

Ruczinski, Ingo ^{[34
]}

Suktitipat, Bhoom ^{[35
]}

Wilson, Alexander F. ^{[33
]}

Yanek, Lisa R. ^{[13
]}

Becker, Lewis C. ^{[13
]}

Linsel-Nitschke, Patrick ^{[11
]}

Lieb, Wolfgang ^{[11
]}

Koenig, Inke R. ^{[12
]}

Hengstenberg, Christian ^{[36
]}

Fischer, Marcus ^{[36
]}

Stark, Klaus ^{[36
]}

Reinhard, Wibke ^{[36
]}

Winogradow, Janina ^{[36
]}

Grassl, Martina ^{[36
]}

机构：

[1] Stanford Univ, Sch Med, Dept Med, Stanford, CA 94304 USA

[2] deCODE Genet, Reykjavik, Iceland

[3] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA

[4] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA

[5] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA

[6] Broad Inst MIT & Harvard, Program Med & Populat Genet, Cambridge, MA USA

[7] Harvard Univ, Sch Med, Dept Med, Boston, MA USA

[8] Univ Penn, Cardiovasc Inst, Philadelphia, PA 19104 USA

[9] Univ Penn, Sch Med, Inst Translat Med & Therapeut, Philadelphia, PA 19104 USA

[10] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA

[11] Univ Lubeck, Med Klin 2, Lubeck, Germany

[12] Univ Lubeck, Inst Med Biometrie & Stat, Lubeck, Germany

[13] Johns Hopkins Sch Med, Dept Med, Baltimore, MD USA

[14] Hamilton Hlth Sci, Populat Hlth Res Inst, Hamilton, ON, Canada

[15] McMaster Univ, Dept Med, Hamilton, ON, Canada

[16] McMaster Univ, Dept Clin Epidemiol & Biostat, Hamilton, ON, Canada

[17] Queens Univ Belfast, Ctr Publ Hlth, Inst Clin Sci, Belfast, Antrim, North Ireland

[18] Vanderbilt Univ, Sch Med, Dept Pediat, Nashville, TN 37212 USA

[19] Washington Hosp Ctr, Cardiovasc Res Inst, MedStar Hlth Res Inst, Washington, DC 20010 USA

[20] Univ Leicester, Dept Hlth Sci, Leicester, Leics, England

[21] HudsonAlpha Inst Biotechnol, Huntsville, AL USA

[22] Kaiser Permanente, Div Res, Oakland, CA USA

[23] Univ Calif San Francisco, Inst Human Genet, San Francisco, CA 94143 USA

[24] Stanford Univ, Dept Genet, Sch Med, Stanford, CA 94305 USA

[25] Univ Munster, Inst Epidemiol & Social Med, Munster, Germany

[26] Univ Munster, Leibniz Inst Arteriosclerosis Res, Munster, Germany

[27] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA

[28] Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC 27710 USA

[29] Univ Iceland, Fac Med, Reykjavik, Iceland

[30] Landspitali Univ Hosp, Dept Med, Reykjavik, Iceland

[31] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland

[32] Johns Hopkins Univ, Sch Med, Dept Anesthesiol & Crit Care Med, Baltimore, MD 21205 USA

[33] NHGRI, Genometr Sect, Inherited Dis Res Branch, NIH, Baltimore, MD USA

[34] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD USA

[35] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA

[36] Univ Regensburg, Klin & Poliklin Innere Med 2, Regensburg, Germany

[37] Univ Kiel, Inst Klin Mol Biol, Kiel, Germany

[38] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Epidemiol, Neuherberg, Germany

[39] Univ Munich, Inst Med Informat Biometry & Epidemiol, Munich, Germany

[40] Univ Munich, Klinikum Grosshadern, D-8000 Munich, Germany

[41] Klinikum Augsburg, KORA Myocardial Infarct Registry, Augsburg, Germany

[42] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA

[43] Univ Washington, Dept Epidemiol, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA

[44] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA

[45] Hebrew Univ Jerusalem, Epidemiol Unit, Hadassah Sch Publ Hlth, Jerusalem, Israel

[46] McGill Univ, Dept Human Genet, Montreal, PQ, Canada

[47] Massachusetts Gen Hosp, Div Gen Med, Dept Med, Boston, MD USA

[48] Brigham & Womens Hosp, Cardiovasc Endocrinol Sect, Div Endocrinol Diabet & Hypertens, Boston, MD USA

[49] Massachusetts Gen Hosp, Ctr Diabet, Boston, MD USA

[50] Childrens Hosp Philadelphia, Ctr Appl Genom, Philadelphia, PA 19104 USA

来源：

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY | 2010年 / 56卷 / 19期

关键词：

coronary artery disease; KIF6; kinesin-like protein 6; myocardial infarction; polymorphism; MYOCARDIAL-INFARCTION; HEART-DISEASE; CARDIOVASCULAR-DISEASE; GENE VARIANTS; RISK-FACTORS; GENOMEWIDE ASSOCIATION; CHROMOSOME; 9P21; EARLY-ONSET; SUSCEPTIBILITY; METAANALYSIS;

D O I：

10.1016/j.jacc.2010.06.022

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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

引用

页码：1552 / 1563

页数：12

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