Inflammatory response and meningioma tumorigenesis and the effect of cyclooxygenase-2 inhibitors

Ragel, Brian T.; Jensen, Randy L.; Couldwell, William T.

doi:10.3171/foc.2007.23.4.8

Cited by 1 publication

(4 citation statements)

References 41 publications

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“…81 Cyclooxygenase-2 (Cox-2) is an inducible enzyme important in mediating inflammatory responses. 95 The role of Cox-2 in tumorigenesis has also previously been demonstrated through its overexpression in colon, lung, and breast cancers. Ragel et al 95 found that Cox-2 is highly and universally expressed in meningiomas.…”

Section: Cyclooxygenase-2mentioning

confidence: 99%

“…95 The role of Cox-2 in tumorigenesis has also previously been demonstrated through its overexpression in colon, lung, and breast cancers. Ragel et al 95 found that Cox-2 is highly and universally expressed in meningiomas. Thus, aberrant activity of eicosanoids may mediate tumor development and growth.…”

Section: Cyclooxygenase-2mentioning

confidence: 99%

“…Treatment with celecoxib demonstrated a dose-dependent growth inhibition of both the IOMM-lee cell line and benign meningioma cells in culture. 95 Celecoxib decreased tumor microvascularity, increased cell apoptosis, and decreased Cox-2 and VEGF expression in vivo in a mouse xenograph model. 96 In addition to Cox-2, Pfister et al 92 identified a number of other potential therapeutic targets involved in eicosanoid formation that are highly expressed in meningiomas, including the enzymes Cox-1, 5-LO, and PTGER4.…”

Section: Targeted Therapiesmentioning

confidence: 99%

“…95 Within the inflammatory pathway, cyclooxygenase serves as the rate-limiting catalyst for the biosynthesis of prostaglandins from arachidonic acid. Prostaglandins, a member of the eicosanoid family of biologically active lipid mediators, regulate a variety of critical cellular processes involved with proliferation, adhesion, angiogenesis, suppression of apoptosis, and inflammation.…”

Section: Cyclooxygenase-2mentioning

confidence: 99%

See 3 more Smart Citations

The molecular genetics and tumor pathogenesis of meningiomas and the future directions of meningioma treatments

Choy

Kim

Nagasawa

et al. 2011

FOC

161

170

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Meningiomas are mostly benign, slow-growing tumors of the CNS that originate from arachnoidal cap cells. While monosomy 22 is the most frequent genetic abnormality found in meningiomas, a multitude of other aberrant chromosomal alterations, signaling pathways, and growth factors have been implicated in its pathogenesis. Losses on 22q12.2, a region encoding the tumor suppressor gene merlin, represent the most common genetic alterations in early meningioma formation. Malignant meningioma progression, however, is associated with more complex karyotypes and greater genetic instability. Cytogenetic studies of atypical and anaplastic meningiomas revealed gains and losses on chromosomes 9, 10, 14, and 18, with amplifications on chromosome 17. However, the specific gene targets in a majority of these chromosomal abnormalities remain elusive. Studies have also implicated a myriad of aberrant signaling pathways involved with meningioma tumorigenesis, including those involved with proliferation, angiogenesis, and autocrine loops. Understanding these disrupted pathways will aid in deciphering the relationship between various genetic changes and their downstream effects on meningioma pathogenesis. Despite advancements in our understanding of meningioma pathogenesis, the conventional treatments, including surgery, radiotherapy, and stereotactic radiosurgery, have remained largely stagnant. Surgery and radiation therapy are curative in the majority of lesions, yet treatment remains challenging for meningiomas that are recurrent, aggressive, or refractory to conventional treatments. Future therapies will include combinations of targeted molecular agents as a result of continued progress in the understanding of genetic and biological changes associated with meningiomas.

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Section: Cyclooxygenase-2mentioning

confidence: 99%

Section: Cyclooxygenase-2mentioning

confidence: 99%