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Validation study of genetic associations with coronary artery disease on chromosome 3q13-21 and potential effect modification by smoking.

Publication ,  Journal Article
Horne, BD; Hauser, ER; Wang, L; Muhlestein, JB; Anderson, JL; Carlquist, JF; Shah, SH; Kraus, WE
Published in: Ann Hum Genet
November 2009

The CATHGEN study reported associations of chromosome 3q13-21 genes (KALRN, MYLK, CDGAP, and GATA2) with early-onset coronary artery disease (CAD). This study attempted to independently validate those associations. Eleven single nucleotide polymorphisms (SNPs) were examined (rs10934490, rs16834817, rs6810298, rs9289231, rs12637456, rs1444768, rs1444754, rs4234218, rs2335052, rs3803, rs2713604) in patients (N = 1618) from the Intermountain Heart Collaborative Study (IHCS). Given the higher smoking prevalence in CATHGEN than IHCS (41% vs. 11% in controls, 74% vs. 29% in cases), smoking stratification and genotype-smoking interactions were evaluated. Suggestive association was found for GATA2 (rs2713604, p = 0.057, OR = 1.2). Among smokers, associations were found in CDGAP (rs10934490, p = 0.019, OR = 1.6) and KALRN (rs12637456, p = 0.011, OR = 2.0) and suggestive association was found in MYLK (rs16834871, p = 0.051, OR = 1.8, adjusting for gender). No SNP association was found among non-smokers, but smoking/SNP interactions were detected for CDGAP (rs10934491, p = 0.017) and KALRN (rs12637456, p = 0.010). Similar differences in SNP effects by smoking status were observed on re-analysis of CATHGEN. CAD associations were suggestive for GATA2 and among smokers significant post hoc associations were found in KALRN, MYLK, and CDGAP. Genetic risk conferred by some of these genes may be modified by smoking. Future CAD association studies of these and other genes should evaluate effect modification by smoking.

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Published In

Ann Hum Genet

DOI

EISSN

1469-1809

Publication Date

November 2009

Volume

73

Issue

Pt 6

Start / End Page

551 / 558

Location

England

Related Subject Headings

  • Smoking
  • Polymorphism, Single Nucleotide
  • Middle Aged
  • Male
  • Humans
  • Genome-Wide Association Study
  • Genetics & Heredity
  • Gene Frequency
  • Female
  • Coronary Artery Disease
 

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Chicago
ICMJE
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Horne, B. D., Hauser, E. R., Wang, L., Muhlestein, J. B., Anderson, J. L., Carlquist, J. F., … Kraus, W. E. (2009). Validation study of genetic associations with coronary artery disease on chromosome 3q13-21 and potential effect modification by smoking. Ann Hum Genet, 73(Pt 6), 551–558. https://doi.org/10.1111/j.1469-1809.2009.00540.x
Horne, Benjamin D., Elizabeth R. Hauser, Liyong Wang, Joseph B. Muhlestein, Jeffrey L. Anderson, John F. Carlquist, Svati H. Shah, and William E. Kraus. “Validation study of genetic associations with coronary artery disease on chromosome 3q13-21 and potential effect modification by smoking.Ann Hum Genet 73, no. Pt 6 (November 2009): 551–58. https://doi.org/10.1111/j.1469-1809.2009.00540.x.
Horne BD, Hauser ER, Wang L, Muhlestein JB, Anderson JL, Carlquist JF, et al. Validation study of genetic associations with coronary artery disease on chromosome 3q13-21 and potential effect modification by smoking. Ann Hum Genet. 2009 Nov;73(Pt 6):551–8.
Horne, Benjamin D., et al. “Validation study of genetic associations with coronary artery disease on chromosome 3q13-21 and potential effect modification by smoking.Ann Hum Genet, vol. 73, no. Pt 6, Nov. 2009, pp. 551–58. Pubmed, doi:10.1111/j.1469-1809.2009.00540.x.
Horne BD, Hauser ER, Wang L, Muhlestein JB, Anderson JL, Carlquist JF, Shah SH, Kraus WE. Validation study of genetic associations with coronary artery disease on chromosome 3q13-21 and potential effect modification by smoking. Ann Hum Genet. 2009 Nov;73(Pt 6):551–558.
Journal cover image

Published In

Ann Hum Genet

DOI

EISSN

1469-1809

Publication Date

November 2009

Volume

73

Issue

Pt 6

Start / End Page

551 / 558

Location

England

Related Subject Headings

  • Smoking
  • Polymorphism, Single Nucleotide
  • Middle Aged
  • Male
  • Humans
  • Genome-Wide Association Study
  • Genetics & Heredity
  • Gene Frequency
  • Female
  • Coronary Artery Disease