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Zeilinger, S. ; Kühnel, B. ; Klopp, N. ; Baurecht, H.* ; Kleinschmidt, A. ; Gieger, C. ; Weidinger, S.* ; Lattka, E. ; Adamski, J. ; Peters, A. ; Strauch, K. ; Waldenberger, M. ; Illig, T.

Tobacco smoking leads to extensive genome-wide changes in DNA methylation.

PLoS ONE 8:e63812 (2013)
Verlagsversion PDF DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Environmental factors such as tobacco smoking may have long-lasting effects on DNA methylation patterns, which might lead to changes in gene expression and in a broader context to the development or progression of various diseases. We conducted an epigenome-wide association study (EWAs) comparing current, former and never smokers from 1793 participants of the population-based KORA F4 panel, with replication in 479 participants from the KORA F3 panel, carried out by the 450K BeadChip with genomic DNA obtained from whole blood. We observed wide-spread differences in the degree of site-specific methylation (with p-values ranging from 9.31E-08 to 2.54E-182) as a function of tobacco smoking in each of the 22 autosomes, with the percent of variance explained by smoking ranging from 1.31 to 41.02. Depending on cessation time and pack-years, methylation levels in former smokers were found to be close to the ones seen in never smokers. In addition, methylation-specific protein binding patterns were observed for cg05575921 within AHRR, which had the highest level of detectable changes in DNA methylation associated with tobacco smoking (-24.40% methylation; p = 2.54E-182), suggesting a regulatory role for gene expression. The results of our study confirm the broad effect of tobacco smoking on the human organism, but also show that quitting tobacco smoking presumably allows regaining the DNA methylation state of never smokers.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Placental Alkaline-phosphatase ; Hydrocarbon Receptor Repressor ; Ah Dioxin Receptor ; Promoter Methylation ; Population ; Smokers ; Cancer ; Lymphoblasts ; Microarray ; Expression
ISSN (print) / ISBN 1932-6203
Zeitschrift PLoS ONE
Quellenangaben Band: 8, Heft: 5, Seiten: , Artikelnummer: e63812 Supplement: ,
Verlag Public Library of Science (PLoS)
Verlagsort Lawrence, Kan.
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Research Unit Molecular Epidemiology (AME)
Institute of Genetic Epidemiology (IGE)
Institute of Epidemiology II (EPI2)
Molekulare Endokrinologie und Metabolismus (MEM)