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

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Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_4EBB6AEEA1DC
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
A genomewide association study of smoking relapse in four European population-based samples.
Périodique
Psychiatric Genetics
Auteur(s)
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.
ISSN
1473-5873 (Electronic)
ISSN-L
0955-8829
Statut éditorial
Publié
Date de publication
2013
Peer-reviewed
Oui
Volume
23
Numéro
4
Pages
143-152
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
Résumé
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.
Pubmed
Web of science
Création de la notice
02/09/2013 8:54
Dernière modification de la notice
20/08/2019 15:04
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