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      Genome-wide association study identifies common variants associated with circulating vitamin E levels

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          Abstract

          In genome-wide association studies (GWAS) of common genetic variants associated with circulating alpha- and gamma-tocopherol concentrations in two adult cohorts comprising 5006 men of European descent, we observed three loci associated with alpha-tocopherol levels, two novel single-nucleotide polymorphisms (SNPs), rs2108622 on 19pter-p13.11 ( P= 1.7 × 10 −8) and rs11057830 on 12q24.31 ( P= 2.0 × 10 −8) and confirmed a previously reported locus marked by rs964184 on 11q23.3 ( P= 2.7 × 10 −10). The three SNPs have been reported to be associated with lipid metabolism and/or regulation. We replicated these findings in a combined meta-analysis with two independent samples, P= 7.8 × 10 −12 (rs964184 on 11q23.3 near BUD13, ZNF259 and APOA1/C3/A4/A5), P= 1.4 × 10 −10 (rs2108622 on 19pter-p13.11 near CYP4F2) and P= 8.2 × 10 −9 (rs11057830 on 12q24.31 near SCARB1). Combined, these SNPs explain 1.7% of the residual variance in log alpha-tocopherol levels. In one of the two male GWAS cohorts ( n= 992), no SNPs were significantly associated with gamma-tocopherol concentrations after including data from the replication sample for 71 independent SNPs with P< 1 × 10 −4 identified.

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          Newly identified loci that influence lipid concentrations and risk of coronary artery disease.

          Cristen J Willer, Serena Sanna, Anne U. Jackson … (2008)
          To identify genetic variants influencing plasma lipid concentrations, we first used genotype imputation and meta-analysis to combine three genome-wide scans totaling 8,816 individuals and comprising 6,068 individuals specific to our study (1,874 individuals from the FUSION study of type 2 diabetes and 4,184 individuals from the SardiNIA study of aging-associated variables) and 2,758 individuals from the Diabetes Genetics Initiative, reported in a companion study in this issue. We subsequently examined promising signals in 11,569 additional individuals. Overall, we identify strongly associated variants in eleven loci previously implicated in lipid metabolism (ABCA1, the APOA5-APOA4-APOC3-APOA1 and APOE-APOC clusters, APOB, CETP, GCKR, LDLR, LPL, LIPC, LIPG and PCSK9) and also in several newly identified loci (near MVK-MMAB and GALNT2, with variants primarily associated with high-density lipoprotein (HDL) cholesterol; near SORT1, with variants primarily associated with low-density lipoprotein (LDL) cholesterol; near TRIB1, MLXIPL and ANGPTL3, with variants primarily associated with triglycerides; and a locus encompassing several genes near NCAN, with variants strongly associated with both triglycerides and LDL cholesterol). Notably, the 11 independent variants associated with increased LDL cholesterol concentrations in our study also showed increased frequency in a sample of coronary artery disease cases versus controls.
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            Cigarette smoking and serum lipid and lipoprotein concentrations: an analysis of published data.

            J Haddow, David Craig, Glenn E. Palomaki (1989)
            To examine the association between cigarette smoking in adults and serum lipid and lipoprotein concentrations the results of 54 published studies were analysed. Overall, smokers had significantly higher serum concentrations of cholesterol (3.0%), triglycerides (9.1%), very low density lipoprotein cholesterol (10.4%), and low density lipoprotein cholesterol (1.7%) and lower serum concentrations of high density lipoprotein cholesterol (-5.7%) and apolipoprotein AI (-4.2%) compared with nonsmokers. Among non-smokers and light, moderate, and heavy smokers a significant dose response effect was present for cholesterol (0, 1.8, 4.3, and 4.5% respectively), triglycerides (0, 10.7, 11.5, and 18.0%), very low density lipoprotein cholesterol (0, 7.2, 44.4, and 39.0%), low density lipoprotein cholesterol (0, -1.1, 1.4, and 11.0%), high density lipoprotein cholesterol (0, -4.6, -6.3, and -8.9%), and apolipoprotein AI (0, -3.7 and -5.7% in non-smokers and light and heavy smokers). These dose response effects may provide new evidence for a causal relation between exposure to cigarette smoke and changes in serum lipid and lipoprotein concentrations whether as a direct result of physiological changes or of dietary changes induced by smoking. Adequate prospective data to estimate the excess risk of coronary artery disease existed only for cholesterol concentration. When that information was combined with data from the present study, and given that smokers as a group face an average overall excess risk of coronary artery disease of 70%, it was estimated that the observed increased serum cholesterol concentration in smokers may account for at least 9% of that excess risk. Furthermore, the dose response effect of smoking on serum cholesterol concentration suggests a gradient of increased absolute risk of coronary artery disease between light and heavy smokers.
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              Genome-wide association study of renal cell carcinoma identifies two susceptibility loci on 2p21 and 11q13.3.

              Lars Vatten, Simone Benhamou, Joanne Colt … (2011)
              We conducted a two-stage genome-wide association study of renal cell carcinoma (RCC) in 3,772 affected individuals (cases) and 8,505 controls of European background from 11 studies and followed up 6 SNPs in 3 replication studies of 2,198 cases and 4,918 controls. Two loci on the regions of 2p21 and 11q13.3 were associated with RCC susceptibility below genome-wide significance. Two correlated variants (r² = 0.99 in controls), rs11894252 (P = 1.8 × 10⁻⁸) and rs7579899 (P = 2.3 × 10⁻⁹), map to EPAS1 on 2p21, which encodes hypoxia-inducible-factor-2 alpha, a transcription factor previously implicated in RCC. The second locus, rs7105934, at 11q13.3, contains no characterized genes (P = 7.8 × 10⁻¹⁴). In addition, we observed a promising association on 12q24.31 for rs4765623, which maps to SCARB1, the scavenger receptor class B, member 1 gene (P = 2.6 × 10⁻⁸). Our study reports previously unidentified genomic regions associated with RCC risk that may lead to new etiological insights.
              Article 0 comments Cited 92 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Hum Mol Genet
                Journal ID (publisher-id): hmg
                Journal ID (hwp): hmg
                Title: Human Molecular Genetics
                Publisher: Oxford University Press
                ISSN (Print): 0964-6906
                ISSN (Electronic): 1460-2083
                Publication date (Print): 1 October 2011
                Publication date (Electronic): 5 July 2011
                Publication date PMC-release: 5 July 2011
                Volume: 20
                Issue: 19
                Pages: 3876-3883
                Affiliations
                [1 ]Division of Cancer Epidemiology and Genetics and
                [2 ]simpleCore Genotyping Facility, National Cancer Institute, NIH , Bethesda, MD, USA,
                [3 ]simpleInformation Management Services, Inc. , Silver Spring, MD, USA,
                [4 ]simpleInstitute of Biostatistics, School of Life Science, Fudan University , Shanghai, People's Republic of China,
                [5 ]Department of Nutrition,
                [6 ]Program in Molecular and Genetic Epidemiology and
                [7 ]Department of Epidemiology, simpleHarvard School of Public Health , Boston, MA, USA,
                [8 ]Department of Pathology, simpleUniversity of Illinois , Chicago, IL, USA,
                [9 ]Channing Laboratory, simpleBrigham and Women's Hospital, Harvard Medical School , Boston, MA, USA,
                [10 ]simpleMarshfield Clinic Research Foundation , Marshfield, WI, USA,
                [11 ]Department of Chronic Disease Prevention, simpleNational Institute for Health and Welfare , Helsinki, Finland
                Author notes
                [* ]To whom correspondence should be addressed at: Division of Cancer Epidemiology and Genetics, EPS-320, National Cancer Institute, Bethesda, MD 20852, USA. Tel: +1 3015942869; Fax: +1 3014966829; Email: daa@ 123456nih.gov
                Article
                Publisher ID: ddr296
                DOI: 10.1093/hmg/ddr296
                PMC ID: 3168288
                PubMed ID: 21729881
                SO-VID: 23d184ae-a937-47fc-99a9-dd64df47d9ff
                Copyright © Published by Oxford University Press 2011.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited

                History
                Date received : 2 February 2011
                Date revision received : 17 June 2011
                Date accepted : 27 June 2011
                Categories
                Subject: Association Studies Articles

                ScienceOpen disciplines: Genetics
                Data availability:
                ScienceOpen disciplines: Genetics

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