Cyclooxygenase in the Treatment of Glioma: Its Complex Role in Signal Transduction

New, Pamela

doi:10.1177/107327480401100303

Cited by 27 publications

(24 citation statements)

References 87 publications

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“…However, apart from the antibody dependent staining results, as discussed above, the inter-and intra-tumoral heterogeneity in COX-2 expression does question the representational value of one tissue section for the whole tumor, as GBM is known for its pluriform morphology. On the other hand, almost all GBMs showed COX-2 positivity, suggesting that GBM patients might benefit from modulation of the COX-2 pathway by prescription of selective COX-2 inhibitors, which are reported to slow down cell proliferation and which in addition, possess radiosensitizing potential (e.g., Milas 2001;Choy and Milas 2003;Kuipers et al 2003;New 2004;Sminia et al 2005). Recent experimental in vivo studies show a lower tumor incidence and a significant reduction in tumor size after administration of the selective COX-2 inhibitor celecoxib (Nam et al 2004), as well as its radiosensitizing capacity (Davis et al 2004).…”

Section: Clinical Perspectivementioning

confidence: 98%

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Expression of cyclooxygenase-2 and epidermal growth factor receptor in primary and recurrent glioblastoma multiforme

Sminia

Stoter

Valk

et al. 2005

J Cancer Res Clin Oncol

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Section: Clinical Perspectivementioning

confidence: 98%

“…Modification of the irradiation response by radiosensitizers is an approach with great potential in optimization of brain tumor therapy (BTC 2001;Hulshof 2002). Emerging studies suggest the cyclooxygenase-2 (COX-2) pathway to be a promising target for therapeutic intervention (Choy and Milas 2003;Nakata et al 2004;New 2004).…”

Section: Introductionmentioning

confidence: 99%

Expression of cyclooxygenase-2 and epidermal growth factor receptor in primary and recurrent glioblastoma multiforme

Sminia

Stoter

Valk

et al. 2005

J Cancer Res Clin Oncol

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“…colon, gastric, pancreatic) [5], including gliomas [6] and has been associated with high tumor aggressiveness and poor patients' prognosis [7,8]. The COX-2 protein is overexpressed in the majority of gliomas, therefore it is considered to be an attractive therapeutic target [6,8,9].…”

Section: Introductionmentioning

confidence: 99%

Radiosensitizing potential of the selective cyclooygenase-2 (COX-2) inhibitor meloxicam on human glioma cells

et al. 2007

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The COX-2 protein is frequently overexpressed in human malignant gliomas. This expression has been associated with their aggressive growth characteristics and poor prognosis for patients. Targeting the COX-2 pathway might improve glioma therapy. In this study, the effects of the selective COX-2 inhibitor meloxicam alone and in combination with irradiation were investigated on human glioma cells in vitro. A panel of three glioma cell lines (D384, U87 and U251) was used in the experiments from which U87 cells expressed constitutive COX-2. The response to meloxicam and irradiation (dose-range of 0-6 Gy) was determined by the clonogenic assay, cell proliferation was evaluated by growth analysis and cell cycle distribution by FACS. 24-72 h exposure to 250-750 lM meloxicam resulted in a time and dose dependent growth inhibition with an almost complete inhibition after 24 h for all cell lines. Exposure to 750 lM meloxicam for 24 h increased the fraction of cells in the radiosensitive G 2 /M cell cycle phase in D384 (18-27%) and U251 (17-41%) cells. 750 lM meloxicam resulted in radiosensitization of D384 (DMF:2.19) and U87 (DMF:1.25) cells, but not U251 cells (DMF:1.08). The selective COX-2 inhibitor meloxicam exerted COX-2 independent growth inhibition and radiosensitization of human glioma cells.

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“…The highly lethal nature of this tumor results from the acquisition of an invasive phenotype that allows the glioblastoma cells to infiltrate surrounding brain tissue [3]. Because of the complexity of the molecular pathogenesis of this tumor, its therapy will most likely remain multifaceted [4]. Over the last few years, a heightened interest in the role of cyclooxygenase (COX)-2 in neoplasia has emerged.…”

Section: Introductionmentioning

confidence: 99%

The cyclooxygenase inhibitor indomethacin modulates gene expression and represses the extracellular matrix protein laminin γ1 in human glioblastoma cells

Ishibashi

Bottone

Taniura

et al. 2005

Experimental Cell Research

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The induction of cyclooxygenase-2 (COX-2) expression is associated with more aggressive gliomas and poor survival. Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit COX activity and have antitumorigenic properties. In this report, our initial aim was to determine if indomethacin would alter gene expression as measured by suppression subtractive hybridization (SSH). Three up-regulated and four down-regulated genes by indomethacin treatment were identified. Laminin gamma1, an extracellular matrix molecule, was the most significantly repressed gene. The repression of laminin gamma1 by indomethacin was confirmed by Northern and Western blot analyses and occurred in a concentration- and time-dependent manner at the protein level. Among several NSAIDs tested, only sulindac sulfide and indomethacin suppressed laminin gamma1 protein expression, and this repression was observed in both COX-expressing and -deficient cell lines, suggesting that laminin gamma1 repression by COX inhibitors was independent of COX. Indomethacin, at a concentration that represses laminin gamma1, inhibited glioblastoma cell invasion that was partially restored with additional human laminin protein containing gamma1 chain. The repression of laminin gamma1 by NSAIDs may be related to attenuation of invasion of brain tumors. These findings are important in understanding the chemopreventive activity of some NSAIDs and could be relevant for designing therapeutic strategies against glioblastoma.

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Cyclooxygenase in the Treatment of Glioma: Its Complex Role in Signal Transduction

Cited by 27 publications

References 87 publications

Expression of cyclooxygenase-2 and epidermal growth factor receptor in primary and recurrent glioblastoma multiforme

Expression of cyclooxygenase-2 and epidermal growth factor receptor in primary and recurrent glioblastoma multiforme

Radiosensitizing potential of the selective cyclooygenase-2 (COX-2) inhibitor meloxicam on human glioma cells

The cyclooxygenase inhibitor indomethacin modulates gene expression and represses the extracellular matrix protein laminin γ1 in human glioblastoma cells

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