Show simple item record

dc.contributor.authorBeane, Jenniferen_US
dc.contributor.authorSebastiani, Paolaen_US
dc.contributor.authorLiu, Gangen_US
dc.contributor.authorBrody, Jerome S.en_US
dc.contributor.authorLenburg, Marc E.en_US
dc.contributor.authorSpira, Avrumen_US
dc.date.accessioned2012-01-09T14:44:45Z
dc.date.available2012-01-09T14:44:45Z
dc.date.copyright2007
dc.date.issued2007-09-25
dc.identifier.citationBeane, Jennifer, Paola Sebastiani, Gang Liu, Jerome S Brody, Marc E Lenburg, Avrum Spira. "Reversible and Permanent Effects of Tobacco Smoke Exposure on Airway Epithelial Gene Expression" Genome Biology 8(9):R201. (2007)
dc.identifier.issn1465-6914
dc.identifier.urihttp://hdl.handle.net/2144/2794
dc.description.abstractOligonucleotide microarray analysis revealed 175 genes that are differentially expressed in large airway epithelial cells of people who currently smoke compared with those who never smoked, with 28 classified as irreversible, 6 as slowly reversible, and 139 as rapidly reversible. BACKGROUND. Tobacco use remains the leading preventable cause of death in the US. The risk of dying from smoking-related diseases remains elevated for former smokers years after quitting. The identification of irreversible effects of tobacco smoke on airway gene expression may provide insights into the causes of this elevated risk. RESULTS. Using oligonucleotide microarrays, we measured gene expression in large airway epithelial cells obtained via bronchoscopy from never, current, and former smokers (n = 104). Linear models identified 175 genes differentially expressed between current and never smokers, and classified these as irreversible (n = 28), slowly reversible (n = 6), or rapidly reversible (n = 139) based on their expression in former smokers. A greater percentage of irreversible and slowly reversible genes were down-regulated by smoking, suggesting possible mechanisms for persistent changes, such as allelic loss at 16q13. Similarities with airway epithelium gene expression changes caused by other environmental exposures suggest that common mechanisms are involved in the response to tobacco smoke. Finally, using irreversible genes, we built a biomarker of ever exposure to tobacco smoke capable of classifying an independent set of former and current smokers with 81% and 100% accuracy, respectively. CONCLUSION. We have categorized smoking-related changes in airway gene expression by their degree of reversibility upon smoking cessation. Our findings provide insights into the mechanisms leading to reversible and persistent effects of tobacco smoke that may explain former smokers increased risk for developing tobacco-induced lung disease and provide novel targets for chemoprophylaxis. Airway gene expression may also serve as a sensitive biomarker to identify individuals with past exposure to tobacco smoke.en_US
dc.description.sponsorshipDoris Duke Charitable Foundation; National Institutes of Health, National Cancer Institute (R21CA10650, R01CA124640); National Institute of Environmental Health Sciences (U01 ES016035)en_US
dc.language.isoenen_US
dc.publisherBioMed Centralen_US
dc.rightsCopyright 2007 Beane et al; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.en_US
dc.rights.urihttp://creativecommons.org/licenses/by/2.0
dc.titleReversible and Permanent Effects of Tobacco Smoke Exposure on Airway Epithelial Gene Expressionen_US
dc.typearticleen_US
dc.identifier.doi10.1186/gb-2007-8-9-r201
dc.identifier.pubmedid17894889
dc.identifier.pmcid2375039


Files in this item

This item appears in the following Collection(s)

Show simple item record

Copyright 2007 Beane et al; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Except where otherwise noted, this item's license is described as Copyright 2007 Beane et al; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.