COX‐2 and c‐kit expression in canine gliomas |
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Authors: | J. M. Jankovsky K. M. Newkirk M. R. Ilha S. J. Newman |
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Affiliation: | 1. College of Veterinary Medicine, University of Tennessee, Knoxville, TN, USA;2. Department of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN, USA;3. Veterinary Diagnostic and Investigational Laboratory, College of Veterinary Medicine, University of Georgia, Tifton, GA, USA |
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Abstract: | Gliomas are among the most common primary neural tumours of dogs. Cyclooxygenase‐2 (COX‐2) and c‐kit overexpression are associated with increased aggressiveness of gliomas and decreased survival in human beings. COX‐2 is the inducible form of cyclooxygenase, which catalyzes prostaglandin formation and may increase tumour proliferation and angiogenesis. C‐kit is a tyrosine kinase receptor involved in normal cell physiology; c‐kit is upregulated in some canine tumours. In this retrospective study, 20 canine gliomas were identified: 11 (55%) oligodendrogliomas, including 1 anaplastic variant; 1 (5%) oligoastrocytoma; and 8 (40%) astrocytomas, of which 2 were glioblastoma multiforme. None of the gliomas expressed COX‐2. None of the gliomas were immunoreactive for c‐kit, although all three high‐grade tumours had intramural vascular expression. Consequently, COX‐2 inhibitors would likely be ineffective against canine gliomas. C‐kit inhibitors may have an anti‐angiogenic effect in high‐grade gliomas, but would likely be ineffective in low‐ and medium‐grade tumours. |
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Keywords: | astrocytoma canine c‐kit COX‐2 glioma oligodendroglioma |
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