Smokers with and without lung cancer can be distinguished using a new gene-expression based approach, reported researchers from Boston University School of Medicine.
The study led by Avrum Spira, MD, MSc, chief of the section of computational biomedicine in the department of medicine at Boston University School of Medicine, and colleagues revealed that the expression of genes belonging to one specific cancer-related pathway are activated in the cells that line the airway of smokers with lung cancer. Moreover, the gene expression activity in the normal cells of the proximal airway precedes the development of lung cancer and may be reversed with a specific chemopreventive agent that targets this pathway.
“This finding is significant as these cells can be obtained in a relatively noninvasive fashion from the airway of smokers at risk for lung cancer, and does not require invasive sampling of lung tissue where lung tumors normally arise,” said Dr. Spira.
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To validate their findings, the researchers measured the biochemical activity of the pathway in the airway epithelial cells from an independent group of smokers with and without lung cancer. “We found that this PI3K pathway gene expression activity is decreased in the airway of high-risk smokers who had regression of their premalignant lesion following treatment with a potential lung cancer chemopreventive agent known as myo-inositol, and demonstrated that myo-inositol inhibits the PI3K pathway in lung cancer cell lines,” Dr. Spira added.
The data suggest that measuring the identified airway gene expression activity can aid in determining specific cancer pathways that have been deregulated within an individual smoker, allowing customization of a specific drug that will target the pathway to reduce an individual’s risk of lung cancer.
The findings were published in Science Translational Medicine (2010;2(26):26ra25).
