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Tozzi, F.* ; Teumer, A.* ; Munafò, M.* ; Rawal, R. ; Kazeem, G.* ; Gerbaulet, M.* ; McArdle, W.* ; Chilcoat, H.* ; Döring, A. ; Dahmen, N.* ; Mooser, V.* ; Nauck, M.* ; Ring, S.M.* ; Rubio, J.P.* ; Vollenweider, P.* ; Waeber, G.* ; John, U.* ; Völzke, H.* ; Homuth, G.* ; Freyberger, H.J.* ; Völker, U.* ; Davey Smith, G.* ; Gieger, C. ; Preisig, M.* ; Grabe, H.J.*

A genomewide association study of smoking relapse in four European population-based samples.

Psychiatr. Genet. 23, 143-152 (2013)
Publ. Version/Full Text Volltext DOI PMC
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OBJECTIVES: Genomewide association studies (GWAS) have identified clear evidence of genetic markers for nicotine dependence. Other smoking phenotypes have been tested, but the results are less consistent. The tendency to relapse versus the ability to maintain long-term abstinence has received little attention in genetic studies; thus, our aim was to provide a better biological understanding of this phenotype through the identification of genetic loci associated with smoking relapse. METHODS: We carried out a GWAS on data from two European population-based collections, including a total of 835 cases (relapsers) and 990 controls (abstainers). Top-ranked findings from the discovery phase were tested for replication in two additional independent European population-based cohorts. RESULTS: Of the seven top markers from the discovery phase, none were consistently associated with smoking relapse across all samples and none reached genomewide significance. A single-nucleotide polymorphism rs1008509, within the Xylosyltransferase II (XYLT2) gene, was suggestively associated with smoking relapse in the discovery phase (β=-0.504; P=5.6E-06) and in the first replication sample (ALSPAC) (β=-0.27; P=0.004; n=1932), but not in the second sample (KORA) (β=0.19; P=0.138; n=912). We failed to identify an association between loci implicated previously in other smoking phenotypes and smoking relapse. CONCLUSION: Although no genomewide significant findings emerged from this study, we found that loci implicated in other smoking phenotypes were not associated with smoking relapse, which suggests that the neurobiology of smoking relapse and long-term abstinence may be distinct from biological mechanisms implicated in the development of nicotine dependence.
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Publication type Article: Journal article
Document type Scientific Article
Keywords ALSPAC; genetics; KORA; PsyCoLaus; SHIP; smoking; Cardiovascular Risk-factors ; Nicotine Dependence ; Wide Association ; Adult Twins ; Tobacco Use ; Cessation ; Metaanalysis ; Behavior ; Abstinence ; Disease
Language english
Publication Year 2013
HGF-reported in Year 2013
ISSN (print) / ISBN 0955-8829
e-ISSN 1473-5873
Journal Psychiatric Genetics
Quellenangaben Volume: 23, Issue: 4, Pages: 143-152 Article Number: , Supplement: ,
Publisher Lippincott Williams & Wilkins
Reviewing status Peer reviewed
Institute(s) Institute of Genetic Epidemiology (IGE)
Institute of Epidemiology (EPI)
POF-Topic(s) 30501 - Systemic Analysis of Genetic and Environmental Factors that Impact Health
30202 - Environmental Health
Research field(s) Genetics and Epidemiology
PSP Element(s) G-504100-001
G-504000-006
G-504000-002
G-504090-001
PubMed ID 23542338
DOI 10.1097/YPG.0b013e32835fc94b
WOS ID WOS:000323222000001
Scopus ID 84879950223
Erfassungsdatum 2013-07-02
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