Seyed Javad Moghaddam, MD

Airway Inflammation’s Role in Lung Cancer

Many studies have found that smokers with chronic obstructive pulmonary disease (COPD) have an increased risk of lung cancer compared with smokers with comparable cigarette exposure but without the disease. COPD causes inflammation in the lung, which persists even after a person stops smoking. These facts suggest a link between chronic airway inflammation and lung cancer, but the precise way in which the link works is unknown. It may be a genetic variation in the immune system’s inflammatory response to inhaled smoke and to microorganisms that gather in the airways of smokers.

Publications:
Ochoa CE, Mirabolfathinejad, SG, Ruiz VA, Evans SE, Gagea, M, Evans CM, Dickey CF, Moghaddam SJ (2011) Interleukin 6 but Not T helper 2 Cytokines Promotes Lung Carcinogenesis.Cancer Prev Res 4(1):52-64.
Through a Lung Cancer Discovery Award, funded in partnership between the American Lung Association and the LUNGevity Foundation, Dr. Moghaddam used a mouse model to study the mechanism responsible for promotion of lung cancer by airway inflammation. He concentrated on a genetic alteration found in COPD and lung cancer, involving a gene called NF-kB and the protein it produces, interleukin 6 (IL-6). Dr. Moghaddam was able to show that COPD-like airway inflammation promotes lung cancer in a mouse model. He found mice whose NF-kB or IL-6 gene was switched off in the airway had a 70% reduction in the number of tumors induced on the surface of the lung compared with mice whose NF-kB or IL-6 gene was not turned off.

This research could lead to development of antiinflammatory therapy in patients with COPD who are at high risk for lung cancer, and in patients with early stage lung cancer.

Dr. Moghaddam was able to use data from this project to apply for and receive a larger grant on dissecting the role of airway inflammation in lung cancer promotion.