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A blood pressure genetic risk score is a significant predictor of incident cardiovascular events in 32,669 individuals.

https://arctichealth.org/en/permalink/ahliterature115422
Source
Hypertension. 2013 May;61(5):987-94
Publication Type
Article
Date
May-2013
Author
Aki S Havulinna
Johannes Kettunen
Olavi Ukkola
Clive Osmond
Johan G Eriksson
Y Antero Kesäniemi
Antti Jula
Leena Peltonen
Kimmo Kontula
Veikko Salomaa
Christopher Newton-Cheh
Author Affiliation
Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland.
Source
Hypertension. 2013 May;61(5):987-94
Date
May-2013
Language
English
Publication Type
Article
Keywords
Adult
Blood Pressure - genetics
Cardiovascular Diseases - epidemiology - ethnology - genetics
Cohort Studies
Cross-Sectional Studies
Female
Finland - epidemiology
Follow-Up Studies
Genome-Wide Association Study
Genotype
Humans
Hypertension - genetics
Incidence
Longitudinal Studies
Male
Middle Aged
Polymorphism, Single Nucleotide - genetics
Prospective Studies
Retrospective Studies
Risk factors
Abstract
Recent genome-wide association studies have identified genetic variants associated with blood pressure (BP). We investigated whether genetic risk scores (GRSs) constructed of these variants would predict incident cardiovascular disease (CVD) events. We genotyped 32 common single nucleotide polymorphisms in several Finnish cohorts, with up to 32,669 individuals after exclusion of prevalent CVD cases. The median follow-up was 9.8 years, during which 2295 incident CVD events occurred. We created GRSs separately for systolic BP and diastolic BP by multiplying the risk allele count of each single nucleotide polymorphism by the effect size estimated in published genome-wide association studies. We performed Cox regression analyses with and without adjustment for clinical factors, including BP at baseline in each cohort. The results were combined by inverse variance-weighted fixed-effects meta-analysis. The GRSs were strongly associated with systolic BP and diastolic BP, and baseline hypertension (all P
Notes
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Comment In: Hypertension. 2013 May;61(5):961-323509079
PubMed ID
23509078 View in PubMed
Less detail

CHRNA5/CHRNA3 Locus Associates with Increased Mortality among Smokers.

https://arctichealth.org/en/permalink/ahliterature287426
Source
COPD. 2016 Aug;13(4):464-70
Publication Type
Article
Date
Aug-2016
Author
Henna Kupiainen
Mikko Kuokkanen
Jukka Kontto
Jarmo Virtamo
Veikko Salomaa
Ari Lindqvist
Maritta Kilpeläinen
Tarja Laitinen
Source
COPD. 2016 Aug;13(4):464-70
Date
Aug-2016
Language
English
Publication Type
Article
Keywords
Aged
Female
Finland
Genetic Predisposition to Disease
Humans
Logistic Models
Lung Neoplasms - genetics - mortality
Male
Middle Aged
Mortality
Neoplasms - genetics - mortality
Nerve Tissue Proteins - genetics
Polymorphism, Genetic
Polymorphism, Single Nucleotide
Prognosis
Proportional Hazards Models
Pulmonary Disease, Chronic Obstructive - genetics - mortality
Receptors, Nicotinic - genetics
Smoking - genetics - mortality
Abstract
Polymorphisms in the nicotinic acetylcholine receptor gene (CHRNA5/CHRNA3 locus) have been associated with several smoking related traits such as nicotine dependence, cigarette consumption, smoking cessation, lung cancer, and COPD. The aim of this candidate gene study was to study the locus among the Finnish COPD patients and long-term smokers with regard to COPD risk, smoking behavior, cancer, and all-cause mortality. Genotyping of rs1051730, the locus tagging SNP was done in two longitudinal cohorts: Finnish COPD patients (N = 575, 74% men) and long-term smokers, all men (N = 1911). Finnish population sample (N = 1730) was used as controls. The analyses were done using logistic and Cox regression. The main findings were that the minor allele increased the risk of COPD when compared to the Finnish population at large (OR = 1.4, 95% CI 1.2-1.7, p = 3.2 × 10-5). Homozygosity for the risk allele was associated in both cohorts with all-cause mortality (crude HR 2.2, 95% CI 1.2-3.8 and 1.3, 95% CI 1.1-1.5, respectively), with any type of cancer (crude OR 2.3, 95% CI 1.0-5.1) among the COPD patients and with the number of pack-years (crude OR 1.4, 95% CI 1.1-1.9) among the male smokers. CHRNA5/CHRNA3 locus tagged by rs1051730, which has been previously associated with several smoking related diseases was now shown to be associated also with increased all-cause mortality among long-term smokers with or without clinical COPD further emphasizing the clinical importance of the finding.
PubMed ID
26751916 View in PubMed
Less detail

Common genetic variants associated with sudden cardiac death: the FinSCDgen study.

https://arctichealth.org/en/permalink/ahliterature122139
Source
PLoS One. 2012;7(7):e41675
Publication Type
Article
Date
2012
Author
Annukka M Lahtinen
Peter A Noseworthy
Aki S Havulinna
Antti Jula
Pekka J Karhunen
Johannes Kettunen
Markus Perola
Kimmo Kontula
Christopher Newton-Cheh
Veikko Salomaa
Author Affiliation
Research Programs Unit, Molecular Medicine and Department of Medicine, University of Helsinki, Helsinki, Finland.
Source
PLoS One. 2012;7(7):e41675
Date
2012
Language
English
Publication Type
Article
Keywords
Adult
Arrhythmias, Cardiac - complications - genetics
Atrial Fibrillation - complications - genetics
Death, Sudden, Cardiac - epidemiology
Female
Finland - epidemiology
Genetic Predisposition to Disease - genetics
Humans
Male
Meta-Analysis as Topic
Middle Aged
Phenotype
Polymorphism, Single Nucleotide
Risk factors
Abstract
Sudden cardiac death (SCD) accounts for up to half of cardiac mortality. The risk of SCD is heritable but the underlying genetic variants are largely unknown. We investigated whether common genetic variants predisposing to arrhythmia or related electrocardiographic phenotypes, including QT-interval prolongation, are associated with increased risk of SCD.
We studied the association between 28 candidate SNPs and SCD in a meta-analysis of four population cohorts (FINRISK 1992, 1997, 2002 and Health 2000, n?=?27,629) and two forensic autopsy series (The Helsinki Sudden Death Study and The Tampere Autopsy Study, n?=?694). We also studied the association between established cardiovascular risk factors and SCD. Causes of death were reviewed using registry-based health and autopsy data. Cox regression and logistic regression models were adjusted for age, sex, and geographic region. The total number of SCDs was 716. Two novel SNPs were associated with SCD: SCN5A rs41312391 (relative risk [RR] 1.27 per minor T allele, 95% CI 1.11-1.45, P?=?3.4×10(-4)) and rs2200733 in 4q25 (RR 1.28 per minor T allele, 95% CI 1.11-1.48, P?=?7.9×10(-4)). We also replicated the associations for 9p21 (rs2383207, RR 1.13 per G allele, 95% CI 1.01-1.26, P?=?0.036), as well as for male sex, systolic blood pressure, diabetes, cigarette smoking, low physical activity, coronary heart disease, and digoxin use (P
Notes
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PubMed ID
22844511 View in PubMed
Less detail

Common genetic variants, QT interval, and sudden cardiac death in a Finnish population-based study.

https://arctichealth.org/en/permalink/ahliterature135070
Source
Circ Cardiovasc Genet. 2011 Jun;4(3):305-11
Publication Type
Article
Date
Jun-2011
Author
Peter A Noseworthy
Aki S Havulinna
Kimmo Porthan
Annukka M Lahtinen
Antti Jula
Pekka J Karhunen
Markus Perola
Lasse Oikarinen
Kimmo K Kontula
Veikko Salomaa
Christopher Newton-Cheh
Author Affiliation
Cardiovascular Research Center and Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA 02114, USA.
Source
Circ Cardiovasc Genet. 2011 Jun;4(3):305-11
Date
Jun-2011
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Cohort Studies
Cross-Sectional Studies
Death, Sudden, Cardiac
Electrocardiography
Female
Finland
Genotype
Humans
Male
Middle Aged
Polymorphism, Single Nucleotide
Abstract
Although sudden cardiac death (SCD) is heritable, its genetic underpinnings are poorly characterized. The QT interval appears to have a graded relationship to SCD, and 35% to 45% of its variation is heritable. We examined the relationship among recently reported common genetic variants, QT interval, and SCD.
We genotyped 15 common (minor allele frequency >1%) candidate single nucleotide polymorphisms (SNPs), based on association with the QT interval in prior studies, in individuals in 2 cohort studies (Health 2000, n = 6597; Mini-Finland, n = 801). After exclusions, we identified 116 incident SCDs from the remaining sample (n = 6808). We constructed a QT genotype score (QT(score)) using the allele copy number and previously reported effect estimates for each SNP. Cox proportional hazards models adjusting for age, sex, and geographical area were used for time to SCD analyses. The QT(score) was a continuous independent predictor of the heart rate-corrected QT interval (P
Notes
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Comment In: Circ Cardiovasc Genet. 2011 Jun;4(3):221-221673310
PubMed ID
21511878 View in PubMed
Less detail

A common variant near the KCNJ2 gene is associated with T-peak to T-end interval.

https://arctichealth.org/en/permalink/ahliterature126894
Source
Heart Rhythm. 2012 Jul;9(7):1099-103
Publication Type
Article
Date
Jul-2012
Author
Annukka Marjamaa
Lasse Oikarinen
Kimmo Porthan
Samuli Ripatti
Gina Peloso
Peter A Noseworthy
Matti Viitasalo
Markku S Nieminen
Lauri Toivonen
Kimmo Kontula
Leena Peltonen
Aki S Havulinna
Antti Jula
Christopher J O'Donnell
Christopher Newton-Cheh
Markus Perola
Veikko Salomaa
Author Affiliation
Research Program in Molecular Medicine, University of Helsinki, Helsinki, Finland. Annukka.Marjamaa@helsinki.fi
Source
Heart Rhythm. 2012 Jul;9(7):1099-103
Date
Jul-2012
Language
English
Publication Type
Article
Keywords
Adult
Asian Continental Ancestry Group - genetics
DNA Methylation
Electrocardiography
Electrophysiologic Techniques, Cardiac
Female
Finland
GC Rich Sequence - genetics
Genetic Predisposition to Disease - genetics
Genome-Wide Association Study
Heart Conduction System - physiopathology
Humans
Long QT Syndrome - genetics
Male
Middle Aged
Polymorphism, Single Nucleotide
Potassium Channels, Inwardly Rectifying - genetics
Abstract
T-peak to T-end (TPE) interval on the electrocardiogram is a measure of myocardial dispersion of repolarization and is associated with an increased risk of ventricular arrhythmias. The genetic factors affecting the TPE interval are largely unknown.
To identify common genetic variants that affect the duration of the TPE interval in the general population.
We performed a genome-wide association study on 1870 individuals of Finnish origin participating in the Health 2000 Study. The TPE interval was measured from T-peak to T-wave end in leads II, V(2), and V(5) on resting electrocardiograms, and the mean of these TPE intervals was adjusted for age, sex, and Cornell voltage-duration product. We sought replication for a genome-wide significant result in the 3745 subjects from the Framingham Heart Study.
We identified a locus on 17q24 that was associated with the TPE interval. The minor allele of the common variant rs7219669 was associated with a 1.8-ms shortening of the TPE interval (P = 1.1 × 10(-10)). The association was replicated in the Framingham Heart Study (-1.5 ms; P = 1.3 × 10(-4)). The overall effect estimate of rs7219669 in the 2 studies was -1.7 ms (P = 5.7 × 10(-14)). The common variant rs7219669 maps downstream of the KCNJ2 gene, in which rare mutations cause congenital long and short QT syndromes.
The common variant rs7219669 is associated with the TPE interval and is thus a candidate to modify repolarization-related arrhythmia susceptibility in individuals carrying the major allele of this polymorphism.
Notes
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PubMed ID
22342860 View in PubMed
Less detail

Contribution of regulatory and structural variations in APOE to predicting dyslipidemia.

https://arctichealth.org/en/permalink/ahliterature171776
Source
J Lipid Res. 2006 Feb;47(2):318-28
Publication Type
Article
Date
Feb-2006
Author
Jari H Stengård
Sharon L R Kardia
Sara C Hamon
Ruth Frikke-Schmidt
Anne Tybjaerg-Hansen
Veikko Salomaa
Eric Boerwinkle
Charles F Sing
Author Affiliation
National Public Health Institute, Helsinki, Finland.
Source
J Lipid Res. 2006 Feb;47(2):318-28
Date
Feb-2006
Language
English
Publication Type
Article
Keywords
African Americans - genetics
Apolipoproteins E - genetics
Cholesterol - blood
Cholesterol, HDL - blood
Denmark - ethnology
Dyslipidemias - blood - ethnology - genetics
European Continental Ancestry Group - genetics
Exons - genetics
Female
Finland - ethnology
Gene Frequency - genetics
Genotype
Haplotypes - genetics
Humans
Male
Middle Aged
Phenotype
Polymorphism, Genetic - genetics
Polymorphism, Single Nucleotide - genetics
Protein Isoforms - genetics
Risk factors
Sex Factors
Triglycerides - blood
United States
Abstract
The objective of this study was to evaluate 1) whether non single nucleotide polymorphisms-coding (non-cSNP) in the apolipoprotein E gene (APOE) identified by resequencing studies contribute to statistically explaining dyslipidemia if variations in the two cSNPs in exon 4 that define the 2, 3, and 4 alleles are ignored, and 2) whether the contribution of these additional SNPs persists when variations in the cSNPs are considered. We used an ecological, multiple-population, data-mining strategy to identify single-SNP and two-SNP genotypes that distinguish between high and low levels of plasma lipids in three training samples, European-Americans from Rochester, MN, African-Americans from Jackson, MS, and Europeans from North Karelia, Finland. We found that a pair of SNPs located in the 5' region define genotypes A560T832/A560T832, A560T832/A560G832, and A560T832/T560T832, which distinguish between high and low levels of HDL-cholesterol (HDL-C), triglycerides (TG), and/or total cholesterol (T-C). The A560T832/- genotypes predicted high TG and high T-C in both genders in a large independent test sample from Copenhagen, Denmark. Prediction of high T-C in the Danish females was dependent on genotypes defined by the cSNPs. Our study suggests that both regulatory and structural variations should be considered when evaluating the utility of APOE for predicting dyslipidemia in the population at large.
Notes
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PubMed ID
16317171 View in PubMed
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Contributions of 18 additional DNA sequence variations in the gene encoding apolipoprotein E to explaining variation in quantitative measures of lipid metabolism.

https://arctichealth.org/en/permalink/ahliterature189100
Source
Am J Hum Genet. 2002 Sep;71(3):501-17
Publication Type
Article
Date
Sep-2002
Author
Jari H Stengård
Andrew G Clark
Kenneth M Weiss
Sharon Kardia
Deborah A Nickerson
Veikko Salomaa
Christian Ehnholm
Eric Boerwinkle
Charles F Sing
Author Affiliation
National Public Health Institute, Helsinki, Finland. jari.stengard@ktl.fi
Source
Am J Hum Genet. 2002 Sep;71(3):501-17
Date
Sep-2002
Language
English
Publication Type
Article
Keywords
African Continental Ancestry Group - genetics
Alleles
Anthropometry
Apolipoproteins E - classification - genetics
Body constitution
European Continental Ancestry Group - genetics
Exons - genetics
Female
Finland
Gene Frequency
Genetic Variation - genetics
Genotype
Humans
Lipid Metabolism
Male
Minnesota
Mississippi
Phenotype
Polymorphism, Single Nucleotide - genetics
Sex Characteristics
Abstract
Apolipoprotein E (ApoE) is a major constituent of many lipoprotein particles. Previous genetic studies have focused on six genotypes defined by three alleles, denoted epsilon2, epsilon3, and epsilon4, encoded by two variable exonic sites that segregate in most populations. We have reported studies of the distribution of alleles of 20 biallelic variable sites in the gene encoding the ApoE molecule within and among samples, ascertained without regard to health, from each of three populations: African Americans from Jackson, Miss.; Europeans from North Karelia, Finland; and non-Hispanic European Americans from Rochester, Minn. Here we ask (1) how much variation in blood levels of ApoE (lnApoE), of total cholesterol (TC), of high-density lipoprotein cholesterol (HDL-C), and of triglyceride (lnTG) is statistically explained by variation among APOE genotypes defined by the epsilon2, epsilon3, and epsilon4 alleles; (2) how much additional variation in these traits is explained by genotypes defined by combining the two variable sites that define these three alleles with one or more additional variable sites; and (3) what are the locations and relative allele frequencies of the sites that define multisite genotypes that significantly improve the statistical explanation of variation beyond that provided by the genotypes defined by the epsilon2, epsilon3, and epsilon4 alleles, separately for each of the six gender-population strata. This study establishes that the use of only genotypes defined by the epsilon2, epsilon3, and epsilon4 alleles gives an incomplete picture of the contribution that the variation in the APOE gene makes to the statistical explanation of interindividual variation in blood measurements of lipid metabolism. The addition of variable sites to the genotype definition significantly improved the ability to explain variation in lnApoE and in TC and resulted in the explanation of variation in HDL-C and in lnTG. The combination of additional sites that explained the greatest amount of trait variation was different for different traits and varied among the six gender-population strata. The role that noncoding variable sites play in the explanation of pleiotropic effects on different measures of lipid metabolism reveals that both regulatory and structural functional variation in the APOE gene influences measures of lipid metabolism. This study demonstrates that resequencing of the complete gene in a sample of >/=20 individuals and an evaluation of all combinations of the identified variable sites, separately for each population and interacting environmental context, may be necessary to fully characterize the impact that a gene has on variation in related traits of a metabolic system.
Notes
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PubMed ID
12165926 View in PubMed
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C-reactive protein-associated genetic variants and cancer risk: findings from FINRISK 1992, FINRISK 1997 and Health 2000 studies.

https://arctichealth.org/en/permalink/ahliterature141399
Source
Eur J Cancer. 2011 Feb;47(3):404-12
Publication Type
Article
Date
Feb-2011
Author
Katriina Heikkilä
Kaisa Silander
Veikko Salomaa
Pekka Jousilahti
Seppo Koskinen
Eero Pukkala
Markus Perola
Author Affiliation
The National Institute for Health and Welfare, Helsinki, Finland. katriina.heikkila@npeu.ox.ac.uk
Source
Eur J Cancer. 2011 Feb;47(3):404-12
Date
Feb-2011
Language
English
Publication Type
Article
Keywords
Adult
Aged
C-Reactive Protein - genetics
Female
Finland - epidemiology
Genetic markers
Genotype
Heterozygote
Heterozygote Detection
Homozygote
Humans
Male
Middle Aged
Neoplasms - epidemiology - genetics
Polymorphism, Single Nucleotide - genetics
Registries
Risk factors
Abstract
Evidence from prospective observational studies suggests that elevated circulating C-reactive protein (CRP) concentrations are associated with cancer risk, but it is unclear whether this association is causal. In order to examine this, we investigated whether genetic variants that are associated with circulating CRP concentrations are associated with cancer risk.
We pooled data from three population-based prospective Finnish studies: FINRISK 1992 (n = 5289), FINRISK 1997 (n = 7160) and Health 2000 (n = 6299). Cancer cases were identified from cancer registrations. Thirteen CRP-associated SNPs, identified from genome-wide association studies, were genotyped. We examined the associations of the SNPs and cancer risk using Cox, probit and instrumented probit regression models.
Compared to common allele homozygotes, individuals carrying one or two variant T alleles at rs1892534 had 1.05-fold (95% confidence interval (CI): 0.90, 1.23) and 1.2-fold (95% CI: 1.01, 1.42) increased overall cancer risk, respectively. Individuals with one or two variant A alleles at rs1169300 or rs2464196 had approximately 1.5- and 2-fold increased risk of lung cancer, respectively (p trend for both: 0.007). CRP SNPs were not associated with colorectal, prostate or breast cancer risk nor was CRP-associated with the probability of developing cancer in the instrumented probit analyses.
We found some evidence for an association of a small number of CRP-associated SNPs with the overall cancer risk and lung cancer risk. Our instrumental variable analyses provided no clear evidence for a causal association of CRP and cancer. These findings suggest that circulating CRP concentrations are unlikely to have a causal role in cancer.
PubMed ID
20727736 View in PubMed
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Detailed metabolic and genetic characterization reveals new associations for 30 known lipid loci.

https://arctichealth.org/en/permalink/ahliterature128942
Source
Hum Mol Genet. 2012 Mar 15;21(6):1444-55
Publication Type
Article
Date
Mar-15-2012
Author
Taru Tukiainen
Johannes Kettunen
Antti J Kangas
Leo-Pekka Lyytikäinen
Pasi Soininen
Antti-Pekka Sarin
Emmi Tikkanen
Paul F O'Reilly
Markku J Savolainen
Kimmo Kaski
Anneli Pouta
Antti Jula
Terho Lehtimäki
Mika Kähönen
Jorma Viikari
Marja-Riitta Taskinen
Matti Jauhiainen
Johan G Eriksson
Olli Raitakari
Veikko Salomaa
Marjo-Riitta Järvelin
Markus Perola
Aarno Palotie
Mika Ala-Korpela
Samuli Ripatti
Author Affiliation
Institute for Molecular Medicine Finland FIMM, Helsinki University Hospital, FI-00014 University of Helsinki, Helsinki, Finland.
Source
Hum Mol Genet. 2012 Mar 15;21(6):1444-55
Date
Mar-15-2012
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Aged, 80 and over
Case-Control Studies
Child
Cohort Studies
Female
Finland - epidemiology
Follow-Up Studies
Genetic Loci - genetics
Genome-Wide Association Study
Humans
Lipid Metabolism - physiology
Lipoproteins - genetics - metabolism
Longitudinal Studies
Magnetic Resonance Spectroscopy
Male
Metabolic Syndrome X - epidemiology - genetics - metabolism
Metabolomics
Middle Aged
Phenotype
Polymorphism, Single Nucleotide - genetics
Quantitative Trait Loci - genetics
Risk factors
Abstract
Almost 100 genetic loci are known to affect serum cholesterol and triglyceride levels. For many of these loci, the biological function and causal variants remain unknown. We performed an association analysis of the reported 95 lipid loci against 216 metabolite measures, including 95 measurements on lipids and lipoprotein subclasses, obtained via serum nuclear magnetic resonance metabolomics and four enzymatic lipid traits in 8330 individuals from Finland. The genetic variation in the loci was investigated using a dense set of 440 807 directly genotyped and imputed variants around the previously identified lead single nucleotide polymorphisms (SNPs). For 30 of the 95 loci, we identified new metabolic or genetic associations (P
PubMed ID
22156771 View in PubMed
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ESR1 genetic variants, haplotypes and the risk of coronary heart disease and ischemic stroke in the Finnish population: a prospective follow-up study.

https://arctichealth.org/en/permalink/ahliterature145431
Source
Atherosclerosis. 2010 Jul;211(1):200-2
Publication Type
Article
Date
Jul-2010
Author
Tarja Kunnas
Kaisa Silander
Juha Karvanen
Maria Valkeapää
Veikko Salomaa
Seppo Nikkari
Author Affiliation
Department of Medical Biochemistry, Medical School, University of Tampere, and Research Unit of the Laboratory Centre, Tampere University Hospital, Tampere, Finland. tarja.kunnas@uta.fi
Source
Atherosclerosis. 2010 Jul;211(1):200-2
Date
Jul-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Coronary Disease - etiology - genetics
Estrogen Receptor alpha - genetics
Female
Finland
Haplotypes
Humans
Longitudinal Studies
Male
Middle Aged
Polymorphism, Single Nucleotide
Risk
Stroke - genetics
Abstract
Association of estrogen receptor 1 (ESR1) gene variants and risk of coronary heart disease (CHD) and ischemic stroke was evaluated in the FINRISK-study. From 14,140 individuals, 2225 were selected for genotyping using a case-cohort design. Time-to-event analysis showed that the CC genotype of -397T/C ERS1 gene contributed to higher risk of CHD only in men (HR, 1.68, CI 1.03-2.74). The -351A/G polymorphism was not independently associated with CHD. Haplotype analysis of these two variants indicated that in men, haplotype TA conferred lower risk of CHD (HR=0.72, CI 0.55-0.95), whereas men with haplotype CA had 1.8 higher risk of CHD events (CI 1.21-2.77), compared to other haplotypes. No association was found with ischemic stroke. Our study suggests that the minor allele -397C of the ESR1 gene confers risk of CHD among Finnish men, both in homozygous state and as part of a haplotype with the -351A allele.
PubMed ID
20153472 View in PubMed
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