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Association between a 15q25 gene variant, nicotine-related habits, lung cancer and COPD among 56,307 individuals from the HUNT study in Norway.

https://arctichealth.org/en/permalink/ahliterature116014
Source
Eur J Hum Genet. 2013 Nov;21(11):1293-9
Publication Type
Article
Date
Nov-2013
Author
Maiken E Gabrielsen
Pål Romundstad
Arnulf Langhammer
Hans E Krokan
Frank Skorpen
Author Affiliation
Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Source
Eur J Hum Genet. 2013 Nov;21(11):1293-9
Date
Nov-2013
Language
English
Publication Type
Article
Keywords
Alleles
Chromosomes, Human, Pair 15 - genetics
Female
Genetic Association Studies
Genetic Predisposition to Disease
Genetic Variation
Humans
Lung - pathology - physiopathology
Lung Neoplasms - complications - genetics - physiopathology
Male
Middle Aged
Norway
Odds Ratio
Polymorphism, Single Nucleotide - genetics
Proportional Hazards Models
Pulmonary Disease, Chronic Obstructive - complications - genetics - physiopathology
Smoking - genetics
Tobacco Use Disorder - complications - genetics - physiopathology
Tobacco, Smokeless
Abstract
Genetic studies have shown an association between single-nucleotide polymorphisms on chromosome 15q25 and smoking-related traits and diseases, such as quantity of smoking, lung cancer and chronic obstructive pulmonary disease (COPD). A discussion has centred on the variants and their effects being directly disease related or indirect via nicotine addiction. To address these discrepancies, we genotyped the single-nucleotide polymorphism rs16969968 in the CHRNA5/A3/B4 gene cluster at chromosome 15q25, in 56?307 individuals from a large homogenous population-based cohort, the North Tr?ndelag Health Study (HUNT) in Norway. The variant was examined in relation to four different outcomes: lung cancer, loss of lung function equivalent to that of COPD, smoking behaviour and the use of smokeless tobacco (snus). Novel associations were found between rs16969968 and the motivational factor for starting to use snus, and the quantity of snus used. Our results also confirm and extend previous findings for associations between rs16969968 and lung cancer, loss of lung function equivalent to that of COPD, and smoking quantity. Our data suggest a role for rs16969968 in nicotine addiction, and the novel association with snus strengthens this observation.
Notes
Cites: Int J Epidemiol. 2010 Apr;39(2):563-7719776245
Cites: Int J Epidemiol. 2010 Apr;39(2):577-920123949
Cites: Nat Genet. 2010 May;42(5):448-5320418888
Cites: Nat Genet. 2010 May;42(5):436-4020418889
Cites: Nat Genet. 2010 May;42(5):441-720418890
Cites: PLoS Genet. 2010 Aug;6(8). pii: e1001053. doi: 10.1371/journal.pgen.100105320700436
Cites: Hum Mol Genet. 2010 Sep 15;19(18):3652-6120587604
Cites: Oncogene. 2010 Sep 2;29(35):4874-8420581870
Cites: Prog Neurobiol. 2010 Oct;92(2):212-2620685379
Cites: Genes Brain Behav. 2010 Oct;9(7):741-5020584212
Cites: Addiction. 2011 Jan;106(1):162-720883459
Cites: PLoS One. 2011;6(4):e1908521559498
Cites: Biochem Pharmacol. 2011 Oct 15;82(8):1015-2121640716
Cites: J Natl Cancer Inst. 2010 Jul 7;102(13):959-7120548021
Cites: Int J Epidemiol. 2013 Aug;42(4):968-7722879362
Cites: Tidsskr Nor Laegeforen. 2002 Sep 30;122(23):2258-6212448263
Cites: J Clin Invest. 2003 Jan;111(1):81-9012511591
Cites: Eur Respir J. 2003 Jun;21(6):1017-2312797498
Cites: Tob Control. 2003 Dec;12(4):349-5914660766
Cites: FASEB J. 1993 Aug;7(11):1045-518370474
Cites: Cell Growth Differ. 1994 Oct;5(10):1033-407848904
Cites: Biochem Pharmacol. 1998 May 1;55(9):1377-8410076528
Cites: Carcinogenesis. 2005 Jul;26(7):1182-9515790591
Cites: Thorax. 2005 Jul;60(7):570-515994265
Cites: Nicotine Tob Res. 2006 Jun;8(3):339-5116801292
Cites: Ann Trop Med Parasitol. 2006 Jul-Sep;100(5-6):481-9916899150
Cites: Nicotine Tob Res. 2011 Dec;13(12):1167-7522071378
Cites: Eur Respir J. 2001 Nov;18(5):770-911757626
Cites: Cell Cycle. 2006 Oct;5(20):2324-817102610
Cites: Hum Mol Genet. 2007 Jan 1;16(1):36-4917135278
Cites: Hum Mol Genet. 2007 Jan 1;16(1):24-3517158188
Cites: Trends Pharmacol Sci. 2008 Mar;29(3):151-818262664
Cites: Mol Psychiatry. 2008 Apr;13(4):368-7318227835
Cites: Nature. 2008 Apr 3;452(7187):633-718385738
Cites: Nature. 2008 Apr 3;452(7187):638-4218385739
Cites: Nat Genet. 2008 May;40(5):616-2218385676
Cites: PLoS Genet. 2008 Jul;4(7):e100012518618000
Cites: Mutat Res. 2008 Sep-Oct;659(3):221-3118495523
Cites: Am J Psychiatry. 2008 Sep;165(9):1163-7118519524
Cites: Eur Respir J. 2008 Nov;32(5):1158-6418978134
Cites: J Natl Cancer Inst. 2008 Nov 5;100(21):1552-618957677
Cites: Nat Genet. 2008 Dec;40(12):1407-918978787
Cites: Nat Rev Cancer. 2009 Mar;9(3):195-20519194381
Cites: PLoS Genet. 2009 Mar;5(3):e100042119300482
Cites: Am J Med Genet B Neuropsychiatr Genet. 2009 Jun 5;150B(4):453-6619259974
Cites: Nicotine Tob Res. 2009 Jul;11(7):785-9619436041
Cites: Cancer Res. 2009 Aug 15;69(16):6633-4119654303
Cites: Cancer Res. 2009 Sep 1;69(17):6848-5619706762
Cites: Mol Cancer Res. 2010 Feb;8(2):194-20320124469
PubMed ID
23443019 View in PubMed
Less detail

Associations of serum 25-hydroxyvitamin D level with incidence of lung cancer and histologic types in Norwegian adults: a case-cohort analysis of the HUNT study.

https://arctichealth.org/en/permalink/ahliterature297760
Source
Eur J Epidemiol. 2018 01; 33(1):67-77
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
01-2018
Author
Yi-Qian Sun
Arnulf Langhammer
Chunsen Wu
Frank Skorpen
Yue Chen
Tom Ivar Lund Nilsen
Pål Richard Romundstad
Xiao-Mei Mai
Author Affiliation
Department of Clinical and Molecular Medicine (IKOM), NTNU, Norwegian University of Science and Technology, Trondheim, Norway. yi-qian.sun@ntnu.no.
Source
Eur J Epidemiol. 2018 01; 33(1):67-77
Date
01-2018
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Adenocarcinoma - blood - epidemiology - pathology
Aged
Aged, 80 and over
Cohort Studies
Female
Humans
Incidence
Lung Neoplasms - blood - epidemiology - pathology
Male
Middle Aged
Norway - epidemiology
Prospective Studies
Vitamin D - analogs & derivatives - blood
Abstract
Previous prospective studies have shown inconsistent associations between serum 25-hydroxyvitamin D [25(OH)D] level and lung cancer incidence. The aim of the present study was to explore the associations of serum 25(OH)D levels with incidence of lung cancer overall and different histologic types. We performed a population-based prospective case-cohort study including 696 incident lung cancer cases and 5804 individuals in a subcohort who participated in the second survey of the Nord-Trøndelag Health Study in Norway. Cox proportional hazards regression models counting for the case-cohort design were used to estimate hazard ratios (HRs) with 95% confidence interval (CIs) for lung cancer overall or histologic types in relation to serum 25(OH)D levels. Compared with the fourth season-specific quartile of 25(OH)D (median 68.0 nmol/L), lower 25(OH)D levels were not associated with the incidence of overall, small or squamous cell lung cancer. However, the risk of adenocarcinoma was lower in the second and third quartiles (median 39.9 and 51.5 nmol/L) compared with the fourth quartile, with HRs of 0.63 (95% CI 0.41-0.98) and 0.58 (0.38-0.88), respectively. The associations of lower levels of 25(OH)D with a reduced risk of adenocarcinoma were only observed in the overweight/obese subjects [HRs for second and third quartiles: 0.40 (0.22-0.72) and 0.50 (0.27-0.92)] but not in the normal weight subjects [HRs: 0.95 (0.52-1.75) and 0.60 (0.32-1.10)]. Serum 25(OH)D levels were not associated with the risk of lung cancer in general. The observation that lower 25(OH)D levels were associated with a lower risk of adenocarcinoma should be interpreted with caution.
PubMed ID
29080012 View in PubMed
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Causal associations of tobacco smoking with cardiovascular risk factors: a Mendelian randomization analysis of the HUNT Study in Norway.

https://arctichealth.org/en/permalink/ahliterature260829
Source
Int J Epidemiol. 2014 Oct;43(5):1458-70
Publication Type
Article
Date
Oct-2014
Author
Bjørn O Åsvold
Johan H Bjørngaard
David Carslake
Maiken E Gabrielsen
Frank Skorpen
George Davey Smith
Pål R Romundstad
Source
Int J Epidemiol. 2014 Oct;43(5):1458-70
Date
Oct-2014
Language
English
Publication Type
Article
Keywords
Alleles
Cardiovascular Diseases - epidemiology - genetics
Causality
Female
Genetic Predisposition to Disease - epidemiology - genetics
Genetic Variation
Humans
Lipids - blood
Male
Mendelian Randomization Analysis
Norway - epidemiology
Population Surveillance
Risk factors
Smoking - epidemiology - genetics
Triglycerides - blood
Waist-Hip Ratio
Abstract
Tobacco smoking has been associated with cardiovascular risk factors including adverse serum lipid levels, central obesity and higher resting heart rate, but lower blood pressure and body mass index (BMI). We used a Mendelian randomization approach to study whether these associations may be causal. If smoking affects cardiovascular risk factors then rs1051730 T alleles, predictors of increased smoking quantity, should be associated with cardiovascular risk factors among smokers, but not among never smokers.
Among 56,625 participants of a population-based study, we estimated associations of rs1051730 T alleles with cardiovascular risk factors and examined whether the associations differed by smoking status.
Rs1051730 T alleles were associated with lower BMI and waist and hip circumferences and higher resting heart rate and estimated glomerular filtration rate (eGFR), and the associations were strongest among current smokers (P interaction 5×10(-9) to 0.01). Rs1051730 T alleles were associated with lower systolic blood pressure and pulse pressure and higher HDL cholesterol concentrations, but these associations did not robustly differ by smoking status. There were no convincing associations of rs1051730 T alleles with waist-hip ratio, diastolic blood pressure and non-fasting serum concentrations of non-HDL cholesterol, triglycerides, glucose and C-reactive protein.
This Mendelian randomization analysis provides evidence that smoking may cause lower BMI and waist and hip circumferences and higher resting heart rate and eGFR. The findings further suggest that smoking is not a major determinant of waist-hip ratio or adverse blood pressure, serum lipid or glucose levels.
Notes
Comment In: Int J Epidemiol. 2014 Oct;43(5):1471-225142441
PubMed ID
24867305 View in PubMed
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Passive smoking in relation to lung cancer incidence and histologic types in Norwegian adults: the HUNT study.

https://arctichealth.org/en/permalink/ahliterature297954
Source
Eur Respir J. 2017 10; 50(4):
Publication Type
Letter
Research Support, Non-U.S. Gov't
Date
10-2017

Prevalence of ZnT8 antibody in relation to phenotype and SLC30A8 polymorphism in adult autoimmune diabetes: results from the HUNT study, Norway.

https://arctichealth.org/en/permalink/ahliterature119907
Source
Autoimmunity. 2013 Feb;46(1):74-9
Publication Type
Article
Date
Feb-2013
Author
Elin Pettersen Sørgjerd
Frank Skorpen
Kirsti Kvaløy
Kristian Midthjell
Valdemar Grill
Author Affiliation
Department of Cancer Research and Molecular Medicine, The Norwegian University of Science and Technology, Levanger, Norway. elin.pettersen@ntnu.no
Source
Autoimmunity. 2013 Feb;46(1):74-9
Date
Feb-2013
Language
English
Publication Type
Article
Keywords
Age of Onset
Cation Transport Proteins - blood - genetics - immunology
Diabetes Mellitus, Type 1 - blood - epidemiology - immunology
Female
Glutamate Decarboxylase - blood - immunology
Humans
Male
Middle Aged
Norway - epidemiology
Phenotype
Polymorphism, Single Nucleotide
Prevalence
Receptor-Like Protein Tyrosine Phosphatases, Class 8 - blood - genetics - immunology
Statistics, nonparametric
Abstract
Zinc transporter 8 (ZnT8), a product of the SLC30A8 gene, is a target-antigen in autoimmune diabetes. Associations between ZnT8 antibody (ZnT8A), phenotype and the genetic variant rs13266634 in the SLC30A8 gene have primarily been studied in patients with young-onset diabetes. We explored such associations in adult-onset autoimmune diabetes identified from the all-population based Nord-Trøndelag health Study (HUNT) ZnT8A (assayed by a fusion probe of C-terminal Arg325 and Trp325), and antibodies against glutamic decarboxylase (GADA) and tyrosine phosphatase-like protein insulinoma antigen-2 (IA-2A) were analysed in 266 subjects classified as having adult-onset autoimmune diabetes ( = 25 years of age at diagnosis). Of these, 161 subjects fulfilled the criteria of latent autoimmune diabetes in adults (LADA), whereas 105 subjects were termed "classical" type 1 diabetes. Ten out of 161 LADA (6.2%) and 23 out of 105 adult-onset "classical" type 1 diabetic patients (22%) were ZnT8A positive. Adult-onset diabetic subjects positive both for GADA and IA-2A (n = 17), had lower waist circumference (p = 0.024) and higher fasting glucose levels (p = 0.023) than those positive both for GADA and ZnT8A (n = 13). Genotyping results of rs13266634 (available in 178 adult-onset diabetic subjects), showed a tendency for association between ZnT8A positivity and the TT- and CC genotypes of SNP rs13266634 (p = 0.101) using the standard cut-off level of 0.06ai, and a significant association at a lower cut-off level of 0.01ai (p = 0.005). We conclude that ZnT8A positivity in a population of adult-onset autoimmune diabetes is a less strong marker of autoimmunity than IA-2A. Further, positivity could be influenced by polymorphism of the SLC30A8 gene.
PubMed ID
23061550 View in PubMed
Less detail

Serum 25-hydroxyvitamin D level, chronic diseases and all-cause mortality in a population-based prospective cohort: the HUNT Study, Norway.

https://arctichealth.org/en/permalink/ahliterature292500
Source
BMJ Open. 2017 Jul 03; 7(6):e017256
Publication Type
Journal Article
Date
Jul-03-2017
Author
Yi-Qian Sun
Arnulf Langhammer
Frank Skorpen
Yue Chen
Xiao-Mei Mai
Author Affiliation
Department of Laboratory Medicine, Children's and Women's Health (LBK), Trondheim, Norway.
Source
BMJ Open. 2017 Jul 03; 7(6):e017256
Date
Jul-03-2017
Language
English
Publication Type
Journal Article
Keywords
Adult
Aged
Chronic Disease - epidemiology
Female
Humans
Male
Middle Aged
Mortality
Norway - epidemiology
Proportional Hazards Models
Prospective Studies
Registries
Risk factors
Vitamin D - analogs & derivatives - blood
Young Adult
Abstract
To investigate the association of vitamin D status with all-cause mortality in a Norwegian population and the potential influences of existing chronic diseases on the association.
A population-based prospective cohort study.
Nord-Trøndelag County, Norway.
A random sample (n=6613) of adults aged 20 years or older in a cohort.
Serum 25-hydroxyvitamin D (25(OH)D) levels were measured in blood samples collected at baseline (n=6377). Mortality was ascertained from the Norwegian National Registry. Cox regression models were applied to estimate the HRs with 95% CIs for all-cause mortality in association with serum 25(OH)D levels after adjustment for a wide spectrum of confounding factors as well as chronic diseases at baseline.
The median follow-up time was 18.5 years, during which 1539 subjects died. The HRs for all-cause mortality associated with the first quartile level of 25(OH)D (
Notes
Cites: Thorax. 2013 Jan;68(1):25-30 PMID 22977130
Cites: Science. 2012 Sep 21;337(6101):1476-8 PMID 22997323
Cites: N Engl J Med. 2007 Jul 19;357(3):266-81 PMID 17634462
Cites: Am J Clin Nutr. 2012 Jan;95(1):91-100 PMID 22170374
Cites: Annu Rev Med. 2016;67:261-72 PMID 26768241
Cites: J Steroid Biochem Mol Biol. 2014 Oct;144 Pt A:138-45 PMID 24239505
Cites: Ann Intern Med. 2012 May 1;156(9):627-34 PMID 22547472
Cites: PLoS One. 2017 Feb 16;12 (2):e0170791 PMID 28207791
Cites: J Bone Miner Res. 2014 Aug;29(8):1709-14 PMID 24737265
Cites: Science. 2015 Jan 23;347(6220):1260419 PMID 25613900
Cites: Am J Clin Nutr. 2013 Apr;97(4):782-93 PMID 23446902
Cites: Nat Biotechnol. 2010 Dec;28(12):1248-50 PMID 21139605
Cites: Int J Epidemiol. 2011 Aug;40(4):998-1005 PMID 21266455
Cites: BMJ. 2014 Nov 18;349:g6330 PMID 25406188
Cites: World Health Organ Tech Rep Ser. 2000;894:i-xii, 1-253 PMID 11234459
Cites: Genome Res. 2010 Oct;20(10):1352-60 PMID 20736230
Cites: Science. 2012 Nov 16;338(6109):883 PMID 23161977
Cites: Nat Rev Cancer. 2014 May;14 (5):342-57 PMID 24705652
Cites: Endocrine. 2016 Feb;51(2):201-2 PMID 26718192
Cites: BMC Med Res Methodol. 2012 Sep 14;12:143 PMID 22978749
Cites: Am J Public Health. 2014 Aug;104(8):e43-50 PMID 24922127
Cites: Cochrane Database Syst Rev. 2014 Jan 10;(1):CD007470 PMID 24414552
Cites: Am J Clin Nutr. 2008 Apr;87(4):1087S-91S PMID 18400739
Cites: Am J Epidemiol. 2010 Apr 15;171(8):903-8 PMID 20219763
Cites: Lancet Diabetes Endocrinol. 2014 Jan;2(1):76-89 PMID 24622671
Cites: PLoS One. 2012;7(11):e48774 PMID 23133659
Cites: BMJ. 2014 Jun 17;348:g3656 PMID 24938302
Cites: Arch Intern Med. 2008 Aug 11;168(15):1629-37 PMID 18695076
Cites: Ageing Res Rev. 2013 Mar;12(2):708-18 PMID 22343489
Cites: BMJ. 2014 Apr 01;348:g1903 PMID 24690623
Cites: Eur J Epidemiol. 2014 Mar;29(3):199-210 PMID 24682834
Cites: Lancet. 2015 Feb 7;385(9967):540-8 PMID 25468166
Cites: BMJ Open. 2016 Nov 18;6(11):e013856 PMID 27864254
PubMed ID
28674149 View in PubMed
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Systematic evaluation of coding variation identifies a candidate causal variant in TM6SF2 influencing total cholesterol and myocardial infarction risk.

https://arctichealth.org/en/permalink/ahliterature104723
Source
Nat Genet. 2014 Apr;46(4):345-51
Publication Type
Article
Date
Apr-2014
Author
Oddgeir L Holmen
He Zhang
Yanbo Fan
Daniel H Hovelson
Ellen M Schmidt
Wei Zhou
Yanhong Guo
Ji Zhang
Arnulf Langhammer
Maja-Lisa Løchen
Santhi K Ganesh
Lars Vatten
Frank Skorpen
Håvard Dalen
Jifeng Zhang
Subramaniam Pennathur
Jin Chen
Carl Platou
Ellisiv B Mathiesen
Tom Wilsgaard
Inger Njølstad
Michael Boehnke
Y Eugene Chen
Gonçalo R Abecasis
Kristian Hveem
Cristen J Willer
Author Affiliation
1] HUNT Research Centre, Department of Public Health and General Practice, Norwegian University of Science and Technology, Levanger, Norway. [2] St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway. [3].
Source
Nat Genet. 2014 Apr;46(4):345-51
Date
Apr-2014
Language
English
Publication Type
Article
Keywords
Animals
Cholesterol, LDL - blood - genetics
Exome - genetics
Gene Knockdown Techniques
Genetic Variation
Genome-Wide Association Study
Genotype
Humans
Lipids - blood - genetics
Membrane Proteins - genetics
Mice
Mice, Inbred C57BL
Mutation, Missense - genetics
Myocardial Infarction - epidemiology - genetics
Norway - epidemiology
Risk factors
Abstract
Blood lipid levels are heritable, treatable risk factors for cardiovascular disease. We systematically assessed genome-wide coding variation to identify new genes influencing lipid traits, fine map known lipid loci and evaluate whether low-frequency variants with large effects exist for these traits. Using an exome array, we genotyped 80,137 coding variants in 5,643 Norwegians. We followed up 18 variants in 4,666 Norwegians and identified ten loci with coding variants associated with a lipid trait (P
PubMed ID
24633158 View in PubMed
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7 records – page 1 of 1.