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GWAS Study

RTN4 and FBXL17 Genes are Associated with Coronary Heart Disease in Genome-Wide Association Analysis of Lithuanian Families.

Domarkienė I, Pranculis A, Germanas S et al.

24778558 PubMed ID
GWAS Study Type
94 Participants
104 Views
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

DI
Domarkienė I
PA
Pranculis A
GS
Germanas S
JA
Jakaitienė A
VD
Vitkus D
DV
Dženkevičiūtė V
KZ
Kučinskienė Z
KV
Kučinskas V
Chapter II

Abstract

Summary of the research findings

Coronary heart disease (CHD) is a complex and heterogeneous cardiovascular disease. There are many genome-wide association studies (GWAS) performed worldwide to extract the causative genetic factors. Moreover, each population may have some exceptional genetic characteristic. Thus, the background of our study is from the previous Lithuanian studies (the LiVicordia Project), which demonstrated the differences of the atherosclerosis process between Lithuanian and Swedish male individuals. In this study we performed GWAS of 32 families of Lithuanian origin in search of significant candidate genetic markers [single nucleotide polymorphisms (SNPs)] of CHD in this population. After careful clinical and biochemical phenotype evaluation, the ∼770K SNPs genotyping (Illumina HumanOmniExpress-12 v1.0 array) and familial GWAS analyses were performed. Twelve SNPs were found to be significantly associated with the CHD phenotype (p value <0.0001; the power >0.65). The odds ratio (OR) values were calculated. Two SNPs (rs17046570 in the RTN4 gene and rs11743737 in the FBXL17 gene) stood out and may prove to be important genetic factors for CHD risk. Our results correspond with the findings in other studies, and these two SNPs may be the susceptibility loci for CHD.

31 European ancestry cases and 63 European ancestry controls from 32 families

Chapter III

Study Statistics

Key metrics and study information

94
Total Participants
GWAS
Study Type
No
Replicated
European
Ancestry
Lithuania
Recruitment Country
Chapter IV

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