1. Cyclooxygenase-2 contributes to mutant epidermal growth factor receptor lung tumorigenesis by promoting an immunosuppressive environment
- Author
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Aidin Iravani, Matthew K. Topham, and Mun Kyoung Kim
- Subjects
biology ,business.industry ,Cell ,Mutant ,General Medicine ,medicine.disease_cause ,medicine.disease ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,lcsh:RC254-282 ,Immune checkpoint ,lung cancer ,medicine.anatomical_structure ,Tumor progression ,egfr ,medicine ,Cancer research ,biology.protein ,Epidermal growth factor receptor ,Cyclooxygenase ,prostaglandin ,Carcinogenesis ,business ,Lung cancer ,cox-2 ,immune checkpoint - Abstract
Targeted therapies reduce growth of mutant epidermal growth factor receptor (EGFR) non-small cell lung cancers, but most patients develop drug resistance. This has led to efforts to develop additional therapies. We found abundant activation of the cyclooxygenase-2 (COX-2) axis in a mouse model of mutant EGFR lung cancer. Inhibiting COX-2 in the mice significantly reduced lung tumor growth, and dual targeting of COX-2 and EGFR had more pronounced effects. Collectively, our data and published data have led us to hypothesize that COX-2 contributes to mutant EGFR lung tumorigenesis, in part, by promoting an immunosuppressive environment that facilitates tumor progression.
- Published
- 2020