We propose that chronic inflammation is an important contributor in the development of lung cancer.
The aims of this research are to establish and characterize a mouse model of chronic airway inflammation that closely resembles the development of emphysema and of lung tumor formation. We will use a transgenic mouse model that inducibly expresses an inflammatory mediator, NF-kB, and in conjunction with the carcinogen, urethane, to model tumor development in the presence of inflammatory mediators. These studies will enable us to define molecular mechanisms by which NF-kB activation in lung epithelium promotes lung tumor formation. Finally, we plan to use the mechanisms defined in these experiments to identify targets for specific treatments aimed at decreasing the development of lung tumor formation in this mouse model. Lung cancer accounts for more cancer related deaths in the United States than the next three leading causes combined. Understanding and defining the molecular mechanisms of the development of lung cancer will lead to new strategies and treatments for lung cancer in the future. ? ? ? ?
