Wahle, Benjamin M.Hawley, Eric T.He, YongzhengSmith, Abbi E.Yuan, JinMasters, Andi R.Jones, David R.Gehlhausen, Jeffrey R.Park, Su-JungConway, Simon J.Clapp, D. WadeYates, Charles W.2018-07-232018-07-232017-10-24Wahle, B. M., Hawley, E. T., He, Y., Smith, A. E., Yuan, J., Masters, A. R., … Yates, C. W. (2018). Chemopreventative celecoxib fails to prevent schwannoma formation or sensorineural hearing loss in genetically engineered murine model of neurofibromatosis type 2. Oncotarget, 9(1), 718–725. http://doi.org/10.18632/oncotarget.22002https://hdl.handle.net/1805/16765Mutations in the tumor suppressor gene NF2 lead to Neurofibromatosis type 2 (NF2), a tumor predisposition syndrome characterized by the development of schwannomas, including bilateral vestibular schwannomas with complete penetrance. Recent work has implicated the importance of COX-2 in schwannoma growth. Using a genetically engineered murine model of NF2, we demonstrate that selective inhibition of COX-2 with celecoxib fails to prevent the spontaneous development of schwannomas or sensorineural hearing loss in vivo, despite elevated expression levels of COX-2 in Nf2-deficient tumor tissue. These results suggest that COX-2 is nonessential to schwannomagenesis and that the proposed tumor suppressive effects of NSAIDs on schwannomas may occur through COX-2 independent mechanisms.en-USAttribution 3.0 United StatesCyclooxygenase 2Neurofibromatosis type 2Non-steroidal anti-inflammatory agentsTransgenic miceVestibular schwannomaArticle