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Conference Paper: A Genome-wide Association Study Identifies a New Genetic Susceptibility Factor for Kawasaki Disease
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TitleA Genome-wide Association Study Identifies a New Genetic Susceptibility Factor for Kawasaki Disease
 
AuthorsDavila, S
Khor, CC
Breunis, WB
Lee, YC
Shimizu, C
Wright, VJ
Yeung, RS
Tan, DEK
Sim, KS
Wang, JJ
Wong, TY
Pang, M
Mitchell, P
Cimaz, R
Dahdah, N
Cheung, YF
Huang, GY
Yang, W
Park, IS
Lee, JK
Wu, JY
Levin, M
Burns, JC
Burgner, D
Kuijpers, TW
Hibberd, ML
 
Issue Date2012
 
PublisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/PED
 
CitationThe 10th International Kawasaki Disease Symposium, Kyoto, Japan, 7-10 February 2012. In Pediatrics International, 2012, v. 54 n. Suppl. 1, p. 45-46, abstract no. O-22 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1442-200X.2012.03534.x
 
AbstractWe performed a case-control GWAS on KD, initially analyzing 494,236 genetic markers in a total of 405 KD cases of European descent matched to 6,252 controls. The independent replication sample set included an additional 1,768 KD cases of European- Caucasian and Asian descent and 3,131 family and population controls in aggregate. The total sample size of 2,173 KD cases and 9,383 controls was assembled by team members from different nations and research networks. Single-SNP analysis for association with KD susceptibility was performed using logistic regression fi tted for genotype trend effects (1 degree of freedom), with adjustment for the top four principal components of population ancestry. We attempted replication of the 62 most signifi cantly associated SNPs in a family-based sample collection of 760 complete parent-offspring trios and 139 discordant sibling pairs using the Sequenom Mass-Array genotyping platform. A total of 5 SNPs showed a consistent direction of effect with the GWAS (1.96 × 10−3 < P < 0.068) in the family-based analysis. Combined analysis of both the GWAS and family-based tests for these 5 SNPs resulted in four exceeding P < 1.0 × 10−5 and representing four distinct genetic loci. We then followed up these SNPs in three Asian collections comprising 438 KD cases vs. 446 controls from Taiwan, 460 KD cases vs. 498 controls from Korea, and 130 KD cases vs. 568 controls from Hong Kong and Shanghai. The specifi c loci and possible functional implications for understanding the immune activation of KD pathogenesis will be discussed.
 
DescriptionConference theme: From Genetics to Clinics
Sesssion: Genetics
 
ISSN1328-8067
2013 Impact Factor: 0.731
 
DOIhttp://dx.doi.org/10.1111/j.1442-200X.2012.03534.x
 
ISI Accession Number IDWOS:000299822300001
 
DC FieldValue
dc.contributor.authorDavila, S
 
dc.contributor.authorKhor, CC
 
dc.contributor.authorBreunis, WB
 
dc.contributor.authorLee, YC
 
dc.contributor.authorShimizu, C
 
dc.contributor.authorWright, VJ
 
dc.contributor.authorYeung, RS
 
dc.contributor.authorTan, DEK
 
dc.contributor.authorSim, KS
 
dc.contributor.authorWang, JJ
 
dc.contributor.authorWong, TY
 
dc.contributor.authorPang, M
 
dc.contributor.authorMitchell, P
 
dc.contributor.authorCimaz, R
 
dc.contributor.authorDahdah, N
 
dc.contributor.authorCheung, YF
 
dc.contributor.authorHuang, GY
 
dc.contributor.authorYang, W
 
dc.contributor.authorPark, IS
 
dc.contributor.authorLee, JK
 
dc.contributor.authorWu, JY
 
dc.contributor.authorLevin, M
 
dc.contributor.authorBurns, JC
 
dc.contributor.authorBurgner, D
 
dc.contributor.authorKuijpers, TW
 
dc.contributor.authorHibberd, ML
 
dc.date.accessioned2012-02-28T01:58:07Z
 
dc.date.available2012-02-28T01:58:07Z
 
dc.date.issued2012
 
dc.description.abstractWe performed a case-control GWAS on KD, initially analyzing 494,236 genetic markers in a total of 405 KD cases of European descent matched to 6,252 controls. The independent replication sample set included an additional 1,768 KD cases of European- Caucasian and Asian descent and 3,131 family and population controls in aggregate. The total sample size of 2,173 KD cases and 9,383 controls was assembled by team members from different nations and research networks. Single-SNP analysis for association with KD susceptibility was performed using logistic regression fi tted for genotype trend effects (1 degree of freedom), with adjustment for the top four principal components of population ancestry. We attempted replication of the 62 most signifi cantly associated SNPs in a family-based sample collection of 760 complete parent-offspring trios and 139 discordant sibling pairs using the Sequenom Mass-Array genotyping platform. A total of 5 SNPs showed a consistent direction of effect with the GWAS (1.96 × 10−3 < P < 0.068) in the family-based analysis. Combined analysis of both the GWAS and family-based tests for these 5 SNPs resulted in four exceeding P < 1.0 × 10−5 and representing four distinct genetic loci. We then followed up these SNPs in three Asian collections comprising 438 KD cases vs. 446 controls from Taiwan, 460 KD cases vs. 498 controls from Korea, and 130 KD cases vs. 568 controls from Hong Kong and Shanghai. The specifi c loci and possible functional implications for understanding the immune activation of KD pathogenesis will be discussed.
 
dc.description.naturelink_to_OA_fulltext
 
dc.descriptionConference theme: From Genetics to Clinics
 
dc.descriptionSesssion: Genetics
 
dc.identifier.citationThe 10th International Kawasaki Disease Symposium, Kyoto, Japan, 7-10 February 2012. In Pediatrics International, 2012, v. 54 n. Suppl. 1, p. 45-46, abstract no. O-22 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1442-200X.2012.03534.x
 
dc.identifier.doihttp://dx.doi.org/10.1111/j.1442-200X.2012.03534.x
 
dc.identifier.epage46, abstract no. O-22
 
dc.identifier.hkuros198737
 
dc.identifier.isiWOS:000299822300001
 
dc.identifier.issn1328-8067
2013 Impact Factor: 0.731
 
dc.identifier.issueSuppl. 1
 
dc.identifier.spage45, abstract no. O-22
 
dc.identifier.urihttp://hdl.handle.net/10722/145609
 
dc.identifier.volume54
 
dc.languageeng
 
dc.publisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/PED
 
dc.publisher.placeAustralia
 
dc.relation.ispartofPediatrics International
 
dc.rightsThe definitive version is available at www3.interscience.wiley.com
 
dc.titleA Genome-wide Association Study Identifies a New Genetic Susceptibility Factor for Kawasaki Disease
 
dc.typeConference_Paper
 
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<contributor.author>Breunis, WB</contributor.author>
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<contributor.author>Shimizu, C</contributor.author>
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<identifier.citation>The 10th International Kawasaki Disease Symposium, Kyoto, Japan, 7-10 February 2012. In Pediatrics International, 2012, v. 54  n. Suppl. 1, p. 45-46, abstract no. O-22</identifier.citation>
<identifier.issn>1328-8067</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/145609</identifier.uri>
<description>Conference theme: From Genetics to Clinics</description>
<description>Sesssion: Genetics</description>
<description.abstract>We performed a case-control GWAS on KD, initially analyzing
494,236 genetic markers in a total of 405 KD cases of European
descent matched to 6,252 controls. The independent replication
sample set included an additional 1,768 KD cases of European-
Caucasian and Asian descent and 3,131 family and population
controls in aggregate. The total sample size of 2,173 KD cases
and 9,383 controls was assembled by team members from different
nations and research networks.
Single-SNP analysis for association with KD susceptibility was
performed using logistic regression fi tted for genotype trend effects (1 degree of freedom), with adjustment for the top four principal
components of population ancestry. We attempted replication of the
62 most signifi cantly associated SNPs in a family-based sample
collection of 760 complete parent-offspring trios and 139 discordant
sibling pairs using the Sequenom Mass-Array genotyping platform.
A total of 5 SNPs showed a consistent direction of effect with the
GWAS (1.96 &#215; 10&#8722;3 &lt; P &lt; 0.068) in the family-based analysis.
Combined analysis of both the GWAS and family-based tests for
these 5 SNPs resulted in four exceeding P &lt; 1.0 &#215; 10&#8722;5 and representing
four distinct genetic loci. We then followed up these SNPs
in three Asian collections comprising 438 KD cases vs. 446
controls from Taiwan, 460 KD cases vs. 498 controls from Korea,
and 130 KD cases vs. 568 controls from Hong Kong and Shanghai.
The specifi c loci and possible functional implications for understanding
the immune activation of KD pathogenesis will be
discussed.</description.abstract>
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