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ß2-adrenergic receptor Thr164Ile polymorphism, obesity, and diabetes: comparison with FTO, MC4R, and TMEM18 polymorphisms in more than 64,000 individuals.

https://arctichealth.org/en/permalink/ahliterature125626
Source
J Clin Endocrinol Metab. 2012 Jun;97(6):E1074-9
Publication Type
Article
Date
Jun-2012
Author
Mette Thomsen
Morten Dahl
Anne Tybjærg-Hansen
Børge G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, Herlev Ringvej 75, DK-2730 Herlev, Denmark.
Source
J Clin Endocrinol Metab. 2012 Jun;97(6):E1074-9
Date
Jun-2012
Language
English
Publication Type
Article
Keywords
Adult
Body mass index
Cohort Studies
Denmark - epidemiology
Diabetes Mellitus - epidemiology - genetics
Female
Genetic Predisposition to Disease - epidemiology - genetics
Genotype
Humans
Male
Membrane Proteins - genetics
Obesity - epidemiology - genetics
Polymorphism, Single Nucleotide - genetics
Proteins - genetics
Receptor, Melanocortin, Type 4 - genetics
Receptors, Adrenergic, beta-2 - genetics
Risk factors
Abstract
The ß(2)-adrenergic receptor (ADRB2) influences regulation of energy balance by stimulating catecholamine-induced lipolysis in adipose tissue. The rare functional ADRB2rs1800888(Thr164Ile) polymorphism could therefore influence risk of obesity and subsequently diabetes.
We tested the hypothesis that the ADRB2rs1800888(Thr164Ile) polymorphism associates with risk of obesity and diabetes and compared effect sizes with those of FTO(rs9939609), MC4R(rs17782313), and TMEM18(rs6548238).
We conducted a population-based cohort study in Copenhagen, Denmark.
We genotyped more than 64,000 individuals from the Danish general population.
We evaluated body mass index (BMI), obesity (BMI =30 kg/m(2)), and diabetes.
Rare allele frequencies were 0.02 for T for ADRB2rs1800888(Thr164Ile), 0.40 for A for FTOrs9939609, 0.25 for C for MC4Rrs17782313, and 0.20 for T for TMEM18rs6548238. For rare vs. common homozygotes, odds ratio for obesity was 3.32 (95% confidence interval = 1.08-10.19) for ADRB2rs1800888(Thr164Ile), 1.42 (1.35-1.52) for FTOrs9939609, 1.18 (1.06-1.30) for MC4Rrs17782313, and 1.28 (1.10-1.50) for TMEM18rs6548238 (common vs. rare). Corresponding odds ratios for diabetes were 1.85 (0.24-14.29), 1.22 (1.07-1.39), 0.96 (0.80-1.16), and 1.61 (1.17-2.22), respectively. After adjustment for BMI, only TMEM18rs6548238 remained associated with diabetes. BMI was increased in rare vs. common homozygotes in FTOrs9939609, MC4Rrs17782313, and TMEM18rs6548238 (common vs. rare) but not in ADRB2rs1800888(Thr164Ile).
Our results suggest that ADRB2rs1800888(Thr164Ile) rare vs. common homozygotes are not significantly associated with an increase in BMI measured continuously but may be associated with an increased risk of obesity. Also, TMEM18rs6548238 associated with risk of diabetes after adjustment for BMI. These findings need confirmation in other studies.
PubMed ID
22466342 View in PubMed
Less detail

Asthma and COPD in cystic fibrosis intron-8 5T carriers. A population-based study.

https://arctichealth.org/en/permalink/ahliterature15007
Source
Respir Res. 2005;6(1):113
Publication Type
Article
Date
2005
Author
Morten Dahl
Anne Tybjaerg-Hansen
Peter Lange
Børge G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry, Herlev University Hospital, DK-2730 Herlev, Denmark. dahlos2003@yahoo.dk
Source
Respir Res. 2005;6(1):113
Date
2005
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Asthma - epidemiology - genetics
Cystic Fibrosis Transmembrane Conductance Regulator - genetics
Denmark - epidemiology
Female
Genetic Predisposition to Disease - epidemiology - genetics
Genetic Screening - methods
Genetics, Population
Heterozygote
Humans
Incidence
Introns - genetics
Male
Middle Aged
Pulmonary Disease, Chronic Obstructive - epidemiology - genetics
Research Support, Non-U.S. Gov't
Risk Assessment - methods
Risk factors
Women
Abstract
BACKGROUND: Carriers of cystic fibrosis intron-8 5T alleles with high exon-9 skipping could have increased annual lung function decline and increased risk for asthma or chronic obstructive pulmonary disease (COPD). METHODS: We genotyped 9131 individuals from the adult Danish population for cystic fibrosis 5T, 7T, 9T, and F508del alleles, and examined associations between 11 different genotype combinations, and annual FEV1 decline and risk of asthma or COPD. RESULTS: 5T heterozygotes vs. 7T homozygous controls had no increase in annual FEV1 decline, self-reported asthma, spirometry-defined COPD, or incidence of hospitalization from asthma or COPD. In 5T/7T heterozygotes vs. 7T homozygous controls we had 90% power to detect an increase in FEV1 decline of 8 ml, an odds ratio for self-reported asthma and spirometry-defined COPD of 1.9 and 1.7, and a hazard ratio for asthma and COPD hospitalization of 1.8 and 1.6, respectively. Both 5T homozygotes identified in the study showed evidence of asthma, while none of four 5T/F508del compound heterozygotes had severe pulmonary disease. 7T/9T individuals had annual decline in FEV1 of 19 ml compared with 21 ml in 7T homozygous controls (t-test: P = 0.03). 6.7% of 7T homozygotes without an F508del allele in the cystic fibrosis transmembrane conductance regulator gene reported asthma vs. 11% of 7T/9T individuals with an F508del allele (chi2: P = 0.01) and 40% of 7T homozygotes with an F508del allele (P = 0.04). 7T homozygotes with vs. without an F508del allele also had higher incidence of asthma hospitalization (log-rank: P = 0.003); unadjusted and adjusted equivalent hazard ratios for asthma hospitalization were 11 (95%CI: 1.5-78) and 6.3 (0.84-47) in 7T homozygotes with vs. without an F508del allele. CONCLUSION: Polythymidine 5T heterozygosity is not associated with pulmonary dysfunction or disease in the adult Caucasian population. Furthermore, our results support that F508del heterozygosity is associated with increased asthma risk independently of the 5T allele.
PubMed ID
16212675 View in PubMed
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Blood pressure, risk of ischemic cerebrovascular and ischemic heart disease, and longevity in alpha(1)-antitrypsin deficiency: the Copenhagen City Heart Study.

https://arctichealth.org/en/permalink/ahliterature53601
Source
Circulation. 2003 Feb 11;107(5):747-52
Publication Type
Article
Date
Feb-11-2003
Author
Morten Dahl
Anne Tybjaerg-Hansen
Henrik Sillesen
Gorm Jensen
Rolf Steffensen
Børge G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry, Herlev University Hospital, Denmark.
Source
Circulation. 2003 Feb 11;107(5):747-52
Date
Feb-11-2003
Language
English
Publication Type
Article
Keywords
Adult
Age Distribution
Aged
Aged, 80 and over
Blood Pressure - genetics
Brain ischemia - epidemiology
Comorbidity
Denmark - epidemiology
Female
Gene Frequency
Genetic Screening
Genotype
Homozygote
Humans
Logistic Models
Male
Middle Aged
Myocardial Ischemia - epidemiology
Odds Ratio
Polymorphism, Genetic
Reference Values
Research Support, Non-U.S. Gov't
Risk assessment
alpha 1-Antitrypsin Deficiency - epidemiology - genetics
Abstract
BACKGROUND: Because elastase in alpha(1)-antitrypsin deficiency may attack elastin in the arterial wall, we tested whether alpha(1)-antitrypsin deficiency is associated with reduced blood pressure, risk of ischemic cerebrovascular (ICVD) and ischemic heart disease (IHD), and longevity. METHODS AND RESULTS: We genotyped 7963 control subjects from the adult general population of Denmark, 1131 Danish patients with ICVD, and 2221 Danish patients with IHD. Compared with MM/MS individuals, systolic blood pressure was lower by 15 mm Hg in ZZ homozygotes (n=6, P=0.03) and 9 mm Hg in MZ heterozygotes with IHD (n=39, P=0.02). Odds ratios for ICVD and IHD in MZ versus MM/MS individuals were 0.70 (0.51 to 0.96) and 0.77 (0.61 to 0.98). Finally, mean ages of MZ and MM/MS control subjects were 58 and 56 years (Mann-Whitney: P=0.008), and relative alpha(1)-antitrypsin MZ genotype frequencies increased from 20 to 93 years among control subjects (chi(2), P=0.002). CONCLUSIONS: ZZ alpha(1)-antitrypsin deficiency and MZ intermediate deficiency in the context of IHD are associated with reduced blood pressure, and MZ is associated with reduced risk of ICVD and IHD. Because MZ heterozygosity was associated with increased age, MZ heterozygosity could be a beneficial condition.
Notes
Comment In: Circulation. 2003 Aug 26;108(8):e62-3; author reply e62-312939251
PubMed ID
12578879 View in PubMed
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Body mass, fat-free body mass, and prognosis in patients with chronic obstructive pulmonary disease from a random population sample: findings from the Copenhagen City Heart Study.

https://arctichealth.org/en/permalink/ahliterature67135
Source
Am J Respir Crit Care Med. 2006 Jan 1;173(1):79-83
Publication Type
Article
Date
Jan-1-2006
Author
Jørgen Vestbo
Eva Prescott
Thomas Almdal
Morten Dahl
Børge G Nordestgaard
Teis Andersen
Thorkild I A Sørensen
Peter Lange
Author Affiliation
Department of Cardiology and Respiratory Medicine, 253 Hvidovre Hospital, Kettegaard Alle 30, DK-2650 Hvidovre, Denmark. joergen.vestbo@hh.hosp.dk
Source
Am J Respir Crit Care Med. 2006 Jan 1;173(1):79-83
Date
Jan-1-2006
Language
English
Publication Type
Article
Keywords
Adiposity
Aged
Body mass index
Body Weight
Cohort Studies
Denmark - epidemiology
Female
Humans
Male
Middle Aged
Prognosis
Pulmonary Disease, Chronic Obstructive - epidemiology
Abstract
RATIONALE: Low body mass index (BMI) is a marker of poor prognosis in chronic obstructive pulmonary disease (COPD). In the general population, the harmful effect of low BMI is due to the deleterious effects of a low fat-free mass index (FFMI; fat-free mass/weight(2)). OBJECTIVES: We explored distribution of low FFMI and its association with prognosis in a population-based cohort of patients with COPD. METHODS: We used data on 1,898 patients with COPD identified in a population-based epidemiologic study in Copenhagen. FFM was measured using bioelectrical impedance analysis. Patients were followed up for a mean of 7 yr and the association between BMI and FFMI and mortality was examined taking age, sex, smoking, and lung function into account. MAIN RESULTS: The mean FFMI was 16.0 kg/m(2) for women and 18.7 kg/m(2) for men. Among subjects with normal BMI, 26.1% had an FFMI lower than the lowest 10th percentile of the general population. BMI and FFMI were significant predictors of mortality, independent of relevant covariates. Being in the lowest 10th percentile of the general population for FFMI was associated with a hazard ratio of 1.5 (95% confidence interval, 1.2-1.8) for overall mortality and 2.4 (1.4-4.0) for COPD-related mortality. FFMI was also a predictor of overall mortality when analyses were restricted to subjects with normal BMI. CONCLUSIONS: FFMI provides information in addition to BMI and assessment of FFM should be considered in the routine assessment of COPD.
Notes
Comment In: Am J Respir Crit Care Med. 2006 Jan 1;173(1):4-516368791
PubMed ID
16368793 View in PubMed
Less detail

Causal and synthetic associations of variants in the SERPINA gene cluster with alpha1-antitrypsin serum levels.

https://arctichealth.org/en/permalink/ahliterature107620
Source
PLoS Genet. 2013;9(8):e1003585
Publication Type
Article
Date
2013
Author
Gian Andri Thun
Medea Imboden
Ilaria Ferrarotti
Ashish Kumar
Ma'en Obeidat
Michele Zorzetto
Margot Haun
Ivan Curjuric
Alexessander Couto Alves
Victoria E Jackson
Eva Albrecht
Janina S Ried
Alexander Teumer
Lorna M Lopez
Jennifer E Huffman
Stefan Enroth
Yohan Bossé
Ke Hao
Wim Timens
Ulf Gyllensten
Ozren Polasek
James F Wilson
Igor Rudan
Caroline Hayward
Andrew J Sandford
Ian J Deary
Beate Koch
Eva Reischl
Holger Schulz
Jennie Hui
Alan L James
Thierry Rochat
Erich W Russi
Marjo-Riitta Jarvelin
David P Strachan
Ian P Hall
Martin D Tobin
Morten Dahl
Sune Fallgaard Nielsen
Børge G Nordestgaard
Florian Kronenberg
Maurizio Luisetti
Nicole M Probst-Hensch
Author Affiliation
Swiss Tropical and Public Health Institute, Basel, Switzerland.
Source
PLoS Genet. 2013;9(8):e1003585
Date
2013
Language
English
Publication Type
Article
Keywords
Denmark
Gene Frequency
Genetic Predisposition to Disease
Genome-Wide Association Study
Genotype
Humans
Lung - pathology
Multigene Family
Polymorphism, Single Nucleotide - genetics
Pulmonary Disease, Chronic Obstructive - blood - genetics - pathology
alpha 1-Antitrypsin - blood - genetics
Abstract
Several infrequent genetic polymorphisms in the SERPINA1 gene are known to substantially reduce concentration of alpha1-antitrypsin (AAT) in the blood. Since low AAT serum levels fail to protect pulmonary tissue from enzymatic degradation, these polymorphisms also increase the risk for early onset chronic obstructive pulmonary disease (COPD). The role of more common SERPINA1 single nucleotide polymorphisms (SNPs) in respiratory health remains poorly understood. We present here an agnostic investigation of genetic determinants of circulating AAT levels in a general population sample by performing a genome-wide association study (GWAS) in 1392 individuals of the SAPALDIA cohort. Five common SNPs, defined by showing minor allele frequencies (MAFs) >5%, reached genome-wide significance, all located in the SERPINA gene cluster at 14q32.13. The top-ranking genotyped SNP rs4905179 was associated with an estimated effect of ß = -0.068 g/L per minor allele (P = 1.20*10(-12)). But denser SERPINA1 locus genotyping in 5569 participants with subsequent stepwise conditional analysis, as well as exon-sequencing in a subsample (N = 410), suggested that AAT serum level is causally determined at this locus by rare (MAF
Notes
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PubMed ID
23990791 View in PubMed
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Change in lung function and morbidity from chronic obstructive pulmonary disease in alpha1-antitrypsin MZ heterozygotes: A longitudinal study of the general population.

https://arctichealth.org/en/permalink/ahliterature67391
Source
Ann Intern Med. 2002 Feb 19;136(4):270-9
Publication Type
Article
Date
Feb-19-2002
Author
Morten Dahl
Anne Tybjaerg-Hansen
Peter Lange
Jørgen Vestbo
Børge G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry 54M1, Herlev University Hospital, Herlev Ringvej 75, DK-2730 Herlev, Denmark.
Source
Ann Intern Med. 2002 Feb 19;136(4):270-9
Date
Feb-19-2002
Language
English
Publication Type
Article
Keywords
Adult
Blood Proteins - genetics
Cystic Fibrosis Transmembrane Conductance Regulator
Denmark - epidemiology
Female
Follow-Up Studies
Forced expiratory volume
Heterozygote
Hospitalization - statistics & numerical data
Humans
Male
Mutation
Pulmonary Disease, Chronic Obstructive - enzymology - genetics - mortality - physiopathology
Questionnaires
Regression Analysis
Research Support, Non-U.S. Gov't
Smoking - adverse effects
Spirometry
alpha 1-Antitrypsin Deficiency - blood - genetics
Abstract
BACKGROUND: A deteriorating effect of severe alpha(1)-antitrypsin deficiency (ZZ genotype) on lung function is well known, whereas the role of intermediate deficiency (MZ genotype) remains uncertain. OBJECTIVE: To test the hypothesis that MZ intermediate alpha(1)-antitrypsin deficiency affects pulmonary function and disease. DESIGN: Population-based cohort study with 21-year follow-up. SETTING: Copenhagen, Denmark. PARTICIPANTS: 9187 adults randomly selected from the Danish general population. MEASUREMENTS: Plasma alpha(1)-antitrypsin levels, annual decrease in FEV(1), airway obstruction, and hospitalization and mortality from chronic obstructive pulmonary disease (COPD). RESULTS: 451 participants (4.9%) carried the MZ genotype. Plasma alpha(1)-antitrypsin levels were 31% lower in MZ heterozygotes than in persons with the MM genotype (Student t -test, P
Notes
SummaryForPatientsIn: Ann Intern Med. 2002 Feb 19;136(4):I3511848738
PubMed ID
11848724 View in PubMed
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Characteristics of undertreatment in COPD in the general population.

https://arctichealth.org/en/permalink/ahliterature107625
Source
Chest. 2013 Dec;144(6):1811-8
Publication Type
Article
Date
Dec-2013
Author
Truls S Ingebrigtsen
Jacob L Marott
Jørgen Vestbo
Jesper Hallas
Børge G Nordestgaard
Morten Dahl
Peter Lange
Source
Chest. 2013 Dec;144(6):1811-8
Date
Dec-2013
Language
English
Publication Type
Article
Keywords
Administration, Inhalation
Adrenal Cortex Hormones - administration & dosage - therapeutic use
Aged
Bronchodilator Agents - administration & dosage - therapeutic use
Cohort Studies
Denmark - epidemiology
Female
Forced Expiratory Volume - physiology
Humans
Male
Middle Aged
Prospective Studies
Pulmonary Disease, Chronic Obstructive - drug therapy - epidemiology - physiopathology
Regression Analysis
Respiratory Function Tests
Retrospective Studies
Severity of Illness Index
Treatment Outcome
Vital Capacity - physiology
Abstract
We wished to characterize undertreatment in COPD.
Among 5,812 individuals with COPD defined by FEV1/FVC < 0.7 participating in the Copenhagen General Population Study, we identified 920 individuals with FEV1 < 60% predicted. Prescriptions were identified in an all-inclusive nationwide registry. For each individual, we examined treatment with medication in the year before the day of the baseline examination, as well as treatment in the first year after the examination. Multivariable logistic regression analyses were applied in individuals with FEV1 < 60% predicted to identify predictors of treatment in the first year after baseline.
Only 30% of individuals with COPD and FEV1 < 60% predicted were treated with medication in the year before the examination, whereas 42.2% were treated with medication in the first year after. Reporting six to 10 previous respiratory infections during the preceding 10 years that required consulting a doctor and/or staying home from work was the strongest predictor of treatment with medication (OR, 7.9; 95% CI, 3.5-19.8; P < .001). Breathlessness, low FEV1, previous admissions with a discharge diagnosis of COPD, and former smoking were also predictors of treatment with medication, whereas comorbidity predicted lack of treatment. In subgroup analysis, among individuals with FEV1 < 50% predicted, visits to the general practitioner and age were additional predictors of treatment, whereas male sex and being a widow/widower predicted lack of treatment.
In this study, we observed important characteristics of a major undertreatment in individuals with COPD in the general population. Previous reported respiratory infections were the strongest predictors of treatment with medications, which indicates that most COPD treatment is initiated because of acute exacerbations.
PubMed ID
23989916 View in PubMed
Less detail

C reactive protein and chronic obstructive pulmonary disease: a Mendelian randomisation approach.

https://arctichealth.org/en/permalink/ahliterature139456
Source
Thorax. 2011 Mar;66(3):197-204
Publication Type
Article
Date
Mar-2011
Author
Morten Dahl
Jørgen Vestbo
Jeppe Zacho
Peter Lange
Anne Tybjærg-Hansen
Børge G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, Herlev Ringvej 75, DK-2730 Herlev, Denmark.
Source
Thorax. 2011 Mar;66(3):197-204
Date
Mar-2011
Language
English
Publication Type
Article
Keywords
Adult
Aged
Biological Markers - blood
C-Reactive Protein - analysis - genetics
Cohort Studies
Denmark - epidemiology
Female
Forced Expiratory Volume - physiology
Genotype
Hospitalization - statistics & numerical data
Humans
Male
Mendelian Randomization Analysis - methods
Middle Aged
Polymorphism, Single Nucleotide
Pulmonary Disease, Chronic Obstructive - blood - epidemiology - genetics - physiopathology
Abstract
It is unclear whether elevated plasma C reactive protein (CRP) is causally related to chronic obstructive pulmonary disease (COPD). The authors tested the hypothesis that genetically elevated plasma CRP causes COPD using a Mendelian randomisation design.
The authors measured high-sensitivity CRP in plasma, genotyped for four single nucleotide polymorphisms in the CRP gene, and screened for spirometry-defined COPD and hospitalisation due to COPD in 7974 individuals from the Copenhagen City Heart Study and in 32,652 individuals from the Copenhagen General Population Study.
Elevated plasma CRP >3 mg/l compared with
PubMed ID
21059738 View in PubMed
Less detail

Elevated ACE activity is not associated with asthma, COPD, and COPD co-morbidity.

https://arctichealth.org/en/permalink/ahliterature151118
Source
Respir Med. 2009 Sep;103(9):1286-92
Publication Type
Article
Date
Sep-2009
Author
Julie Lee
Børge G Nordestgaard
Morten Dahl
Author Affiliation
Department of Clinical Biochemistry 54M1, Herlev University Hospital, Herlev Ringvej 75, Herlev, Denmark.
Source
Respir Med. 2009 Sep;103(9):1286-92
Date
Sep-2009
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Asthma - enzymology - genetics
Denmark
Exercise
Female
Gene Frequency
Genetic Predisposition to Disease - genetics
Genotype
Humans
Male
Middle Aged
Odds Ratio
Peptidyl-Dipeptidase A - genetics - metabolism
Pulmonary Disease, Chronic Obstructive - enzymology - genetics
Risk assessment
Young Adult
Abstract
The angiotensin-converting enzyme (ACE) gene is a potential candidate gene for risk of asthma, COPD, and COPD co-morbidity. In 9034 Danish adults, we determined whether individuals homozygous or heterozygous for the ACE D allele are at greater risk of asthma, COPD, or COPD co-morbidity compared with ACE II homozygous individuals. In the general population, serum ACE activity increased with the number of D alleles (Kruskal-Wallis ANOVA: II vs. ID, p
PubMed ID
19423314 View in PubMed
Less detail

Genetically lowered microsomal epoxide hydrolase activity and tobacco-related cancer in 47,000 individuals.

https://arctichealth.org/en/permalink/ahliterature133868
Source
Cancer Epidemiol Biomarkers Prev. 2011 Aug;20(8):1673-82
Publication Type
Article
Date
Aug-2011
Author
Julie Lee
Morten Dahl
Børge G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry, Herlev Hospital, Herlev, Denmark.
Source
Cancer Epidemiol Biomarkers Prev. 2011 Aug;20(8):1673-82
Date
Aug-2011
Language
English
Publication Type
Article
Keywords
Aged
Cocarcinogenesis
Denmark - epidemiology
Epoxide Hydrolases - genetics - metabolism
Female
Genetic Predisposition to Disease
Genotype
Humans
Male
Middle Aged
Neoplasms - enzymology - epidemiology - etiology - genetics
Questionnaires
Smoking - adverse effects - epidemiology - genetics - metabolism
Abstract
Two functional polymorphisms of the microsomal epoxide hydrolase (mEH) gene (EPHX1), Tyr113His (rs1051740) and His139Arg (rs2234922), have variably been found to influence susceptibility to various cancer forms. We tested whether genetically lowered mEH activity affects risk of developing cancer in the general population.
We genotyped 47,089 individuals from the Danish general population for the Tyr113His and His139Arg polymorphisms in the EPHX1 gene and divided them into groups with predicted fast, intermediate, and slow mEH activity. Using Cox proportional hazards models, we calculated HRs for 26 individual cancer diagnoses and for groups of any cancer, tobacco-related cancers, estrogen-related female cancers, and other cancers.
Of the 47,089 individuals, 7,590 experienced a cancer event, and of these, 1,466 were tobacco-related. After multifactorial adjustment, the HRs (95% CI) for tobacco-related cancer were 1.1 (0.8-1.5) and 1.5 (1.1-2.0) in individuals with intermediate and slow mEH activity versus individuals with the fast phenotype (P(trend) = 0.003). The corresponding HRs among ever-smokers were 1.1 (0.8-1.5) and 1.5 (1.1-2.0; P(trend) = 0.003), whereas HRs among never-smokers did not differ from 1.0.
Our results indicate that genetically lowered mEH activity is associated with increased risk of developing tobacco-related cancer among smokers in the general population; however, additional studies are needed to confirm our findings.
To our knowledge, this is the largest study to investigate the association of mEH phenotype and genotype with tobacco-related cancers combined in the general population.
PubMed ID
21653646 View in PubMed
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