A team at the University of Utah is excited to have found a promising new method to detect lung cancer in its very early stages. Lung cancer is particularly dangerous because it’s so difficult to diagnose early enough to give treatment the best shot at being successful.

The results are exciting in that they suggest that the gene pathway P13K may be a very strong marker for diagnosing lung cancer early on, possibly before tumors have even developed.

Though cigarette smoking is responsible for upwards of 90% of all lung cancer diagnoses, only a relatively small number of smokers actually develop lung cancer, say the study authors. Up till now, researchers haven’t been sure why this is the case, but the new study suggests that changes in a specific gene signaling pathway may be the key.

Adam M. Gustafson and his team write that “the damage caused by cigarette smoke is not limited solely to the lung but rather forms a ‘field of injury’ throughout the entire respiratory tract.” This phenomenon allowed the researchers to use a relatively non-invasive technique called bronchoscopy, in which a sample of cells is taken from the upper airway of the patient. Even though these airway cells looked normal under the microscope, because of miniscule changes at the level of the genes, the researchers hoped that the cells might be accurate predictors of cancerous changes in the lungs themselves.

The team specifically looked at changes in the P13K gene pathway in smokers who had lung cancer and those who did not. They found that, compared to healthy controls, P13K levels were significantly higher in the lung cancer patients, as well as in those who had “dysplastic lesions” but were technically in the precancerous stage. Further, when the cells were treated with myo-inositol, an anticancer agent, the activity of the P13K pathway was significantly reduced.

The results are exciting in that they suggest that the gene pathway P13K may be a very strong marker for diagnosing lung cancer early on, possibly before tumors have even developed. The authors conclude that myo-inositol may be a good treatment option to reverse very early P13K changes: “If the chemo-preventive effects of myo-inositol are confirmed in larger clinical trials, the use of this compound in high-risk smokers with perturbed PI3K activity in the airway could decrease lung cancer occurrence.”

Adam M. Gustafson works in the Department of Medicine and Pulmonary Center at the Boston University Medical Center in Boston, Mass.