Researchers from the Boston University School of Medicine and other institutions have observed a significant increase in genomic activity associated with activation of the phosphatidylinositol 3 kinase (PI3K) pathway in the normal bronchial airway of smokers with lung cancer and smokers with dysplastic lesions (Gustafson AM et al. Sci Transl Med. 2010;2:26ra25). The findings suggest that PI3K is activated in cells of the proximal airway before tumorigenesis.
The investigators also found decreased PI3K activity in the airway of high-risk smokers who had significant regression of dysplasia after treatment with the chemopreventive agent myo-inositol. Myo-inositol also inhibited the PI3K pathway in vitro.
Hampton T. Lung Cancer Pathway. JAMA. 2010;303(21):2129. doi:10.1001/jama.2010.687