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Airway epithelial cell gene expression altered by cigarette smoking

Reuters Health

Posting Date: June 21, 2004

Last Updated: 2004-06-21 17:00:29 -0400 (Reuters Health)

NEW YORK (Reuters Health) - Cigarette smoking alters the gene expression of airway epithelial cells, and some changes do not return to normal after smoking cessation, according to a report in the June 21st PNAS Early Edition.

Few studies have reported how smoking affects airway epithelial cells or how smoking-induced alterations change with smoking cessation, the authors explain.

Dr. Avrum Spira from Boston University School of Medicine, Boston, Massachusetts and colleagues used high-density gene expression arrays to identify genes normally expressed in human airway epithelial cells obtained at bronchoscopy and to determine how gene expression changes with cigarette smoking and whether changes are reversible when smoking is discontinued.

In 34 current smokers, 97 genes were differentially expressed compared to never smokers. According to the results, genes involved in regulating oxidant stress and glutathione metabolism, xenobiotic metabolism, and secretion, as well as several putative oncogenes, were increased. Genes involved in regulating inflammation and several putative tumor suppressor genes were decreased.

Gene expression changes correlated with cumulative cigarette exposure, the investigators report, but age and gender had little effect on smoking-induced changes.

Smokers who had stopped smoking at least 2 years before the study tended to cluster with never smokers, the researchers note, and more recent quitters tended to cluster with current smokers.

Thirteen genes did not return to normal levels in former smokers even after 20 to 30 years of smoking cessation, the report indicates. Among these genes were a number of potential tumor suppressor genes that are permanently decreased and several putative oncogenes that are permanently increased.

"The persistence of abnormal expression of select genes after smoking cessation may provide growth advantages to a subset of epithelial cells, allowing for clonal expansion and perpetuation of these cells years after smoking had been discontinued," the authors suggest. "These permanent changes might explain the persistent risk of lung cancer in former smokers."

"In addition," the investigators conclude, "results from this study raise the possibility that the airway gene expression profile in smokers may serve as a biomarker for lung cancer."

Proc Natl Acad Sci USA 2004.

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