Abstract
Three studies addressed the role of cyclooxygenase-2 (COX-2) in mammary tumorigenesis using epithelial and macrophage COX-2 knockout mice. Deletion of COX-2 in either cell restored, at least partially, tumor immunosurveillance either by changing macrophage function to offset pro-tumor effects, or by attracting more cytotoxic T lymphocytes and natural killer cells to the tumor. These studies suggest benefits from targeted COX-2 selective inhibition in combination with immunotherapies.