Lipopolysaccharide-mediated chronic inflammation promotes tobacco carcinogen-induced lung tumorigenesis

We developed a two-staged lung cancer mouse model, which mimics the smoking carcinogen-induced, and chronic obstructive pulmonary disease (COPD)-related airway inflammation promoted lung cancers. We used the carcinogen 4-(methylnitrosamino)-1-(3- pyridyl)-1-butanone (NNK) to induce lung cancer and in parallel to repeated Lipopolysaccharide (LPS) installation to induce chronic lung inflammation. To identify genes associated with chronic inflammation promoting lung tumorigenesis, we have performed whole genome microarray expression profiling of mice exposed to Phosphate-Buffered Saline (PBS), NNK, LPS, and combined NNK and LPS. Expression profiles of 12 samples in mice treated with PBS (n=3), LPS (n=3), NNK (n=3), and LPS/NNK (n=3)