Inflammatory response and meningioma tumorigenesis and the effect of cyclooxygenase-2 inhibitors.
In this article the authors discuss the rationale and research supporting the hypothesis that meningioma tumorigenesis may, in part, be driven by overexpression of cyclooxygenase-2 (Cox-2) and that treatment with celecoxib, a selective Cox-2 inhibitor, may hold therapeutic promise. Because therapies for recurrent or aggressive meningiomas (atypical or malignant subtypes) such as chemotherapy and radiotherapy generally offer little therapeutic benefit, interest in targeting Cox-2 has grown. This rate-limiting enzyme of prostaglandin synthesis can be inhibited with nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen and celecoxib. Treatment with NSAIDs has been shown to curb the tumorigenic properties of prostaglandins in several cancer models via both Cox-2-dependent and -independent mechanisms. In addition, celecoxib is well tolerated in humans, making its use as a chronic therapy for meningiomas attractive.
Ragel
Brian T
BT
Department of Neurosurgery, University of Utah, Salt Lake City, Utah 94132, USA.
Jensen
Randy L
RL
Couldwell
William T
WT
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D051546:Cyclooxygenase 2 / Q000502:physiology*; D052246:Cyclooxygenase 2 Inhibitors / Q000627:therapeutic use*; D006801:Humans; D007249:Inflammation / Q000473:pathology; D008577:Meningeal Neoplasms / Q000188:drug therapy / Q000209:etiology* / Q000473:pathology; D008579:Meningioma / Q000188:drug therapy / Q000209:etiology* / Q000473:pathology
D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D051546:Cyclooxygenase 2