The B vitamin-related natural substance, myo-inositol is in the news lately. Now new research suggests that changes in a set of genes that are active in smokers who go on to develop lung cancer might offer early detection and even prevention treatments. Once cancer is initiated, the factors that promote it can differ from those that initiate it.
In any event, the gene involved is called PI3K, which interacts with inositol. Patients in a trial of inositol for lung cancer prevention apparently showed reductions in the activation of the PI3K. So, inositol may tell the genetic and cellular changes that precede full expression of lung cancer to stand down and halt their progression toward disease.
Sounds worth exploring. As always, who knows if inositol would have actual clinical benefits and low risk, and it is up to each person at risk of cancer or with cancer now to decide at this point in time if the current unknowns about inositol are worth dealing with sooner rather than later (as usual, myo-inositol is widely available over the counter in health food stores). This is worth a discussion with your doctor, though, if lung cancer (or some other cancers where inositol might be helpful) is a concern for you.
Here’s the whole abstract about this latest study:
Sci Transl Med. 2010 Apr 7;2(26):26ra25.
Airway PI3K Pathway Activation Is an Early and Reversible Event in Lung Cancer Development.
Gustafson AM, Soldi R, Anderlind C, Scholand MB, Qian J, Zhang X, Cooper K, Walker D, McWilliams A, Liu G, Szabo E, Brody J, Massion PP, Lenburg ME, Lam S, Bild AH, Spira A.
Section of Computational Biomedicine, Department of Medicine and Pulmonary Center, Boston University Medical Center, Boston, MA 02118, USA.
Abstract
Although only a subset of smokers develop lung cancer, we cannot determine which smokers are at highest risk for cancer development, nor do we know the signaling pathways altered early in the process of tumorigenesis in these individuals. On the basis of the concept that cigarette smoke creates a molecular field of injury throughout the respiratory tract, this study explores oncogenic pathway deregulation in cytologically normal proximal airway epithelial cells of smokers at risk for lung cancer. We observed a significant increase in a genomic signature of phosphatidylinositol 3-kinase (PI3K) pathway activation in the cytologically normal bronchial airway of smokers with lung cancer and smokers with dysplastic lesions, suggesting that PI3K is activated in the proximal airway before tumorigenesis. Further, PI3K activity is decreased in the airway of high-risk smokers who had significant regression of dysplasia after treatment with the chemopreventive agent myo-inositol, and myo-inositol inhibits the PI3K pathway in vitro. 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. Our work further suggests that additional lung cancer chemoprevention trials either targeting the PI3K pathway or measuring airway PI3K activation as an intermediate endpoint are warranted.
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