But PI3K pathway activity declines in high-risk smokers treated with myo-inositol

-- Beth Gilbert

Thursday, April 8, 2010 (Last Updated: 04/09/2010)

THURSDAY, April 8 (HealthDay News) -- Biochemical signals in the lungs of current and former smokers may help identify those most likely to develop lung cancer, and this sequence of chemical reactions can be reversed before cancer starts by a potential lung cancer drug, according to a study in the April 7 issue of Science Translational Medicine.

Adam M. Gustafson, Ph.D., of the Boston University Medical Center, and colleagues measured the expression of genes from different cancer-related pathways in the lungs of smokers with and without lung cancer, as well as in those at high risk for developing lung cancer.

The researchers found that genes from the phosphatidylinositol 3-kinase (PI3K) pathway were activated to higher levels in the airways of smokers with lung cancer or cancerous lesions than in the airways of smokers who did not develop cancer. In addition, the researchers found that PI3K pathway activity declined in the airways of high-risk smokers who had significant regression of cancerous lesions following treatment with the chemopreventive agent myo-inositol, which blocks the pathway.

"These results suggest that deregulation of the PI3K pathway in the bronchial airway epithelium of smokers is an early, measurable, and reversible event in the development of lung cancer and that genomic profiling of these relatively accessible airway cells may enable personalized approaches to chemoprevention and therapy," the authors write.

Three authors disclosed financial ties to Allegro Diagnostics, which specializes in gene expression molecular diagnostic testing for lung cancer and other diseases. Boston University and the University of Utah have filed a provisional patent related to PI3K gene signature generation and its use.

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Specialties Oncology

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