Recently, scientists found mutations in some lung adenocarcinomas and bronchioloalveolar carcinomas that activate a tumor promoting receptor called EGFR.  We found that these mutations in EGFR caused high expression of another protein called COX-2.  The COX-2 protein can, in turn, activate EGFR, potentially creating a perpetual growth cycle.  COX-2 also promotes inflammation, and in addition to increasing COX-2, mutant EGFR also causes expression of other pro-inflammatory proteins.  Normally, inflammation is appropriate and helps healing, but too much inflammation can cause injury and even promote cancer.  Our findings suggest that in tumors with mutant EGFR, COX-2 and inflammation contribute to tumor growth and maintenance.  We propose to study the role of COX-2 and inflammation in tumors that have EGFR mutations.   If we find that they contribute to tumor growth and maintenance, it might be possible to improve treatment of lung tumors with mutant EGFR by providing anti-inflammatory medications such as the COX-2 inhibitors aspirin, ibuprofen, or Celebrex.