[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 54.146.179.146. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Citations 0
Lab Reports
June 2, 2010

Lung Cancer Pathway

JAMA. 2010;303(21):2129. doi:10.1001/jama.2010.687

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[26]: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.

First Page Preview View Large
First page PDF preview
First page PDF preview
×