Expression of Cyclooxygenase-2 in Canine Renal Cell Carcinoma

Cyclooxygenase-2 (COX-2) has been shown to be the primary enzyme responsible for prostaglandin production during inflammation but is absent in most tissues under normal physiological states. High levels of COX-2 expression have been observed in the macula densa and thick ascending limbs of fetal kid...

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Bibliographic Details
Published in:Veterinary pathology 2001-01, Vol.38 (1), p.116-119
Main Authors: M. Khan, K. N., Stanfield, K. M., Trajkovic, D., Knapp, D. W.
Format: Article
Language:English
Subjects:
Animals
Carcinoma, Renal Cell - enzymology
Carcinoma, Renal Cell - genetics
Carcinoma, Renal Cell - pathology
Carcinoma, Renal Cell - veterinary
Cyclooxygenase 2
Dog Diseases - enzymology
Dog Diseases - genetics
Dog Diseases - pathology
Dogs
Female
Gene Expression Regulation, Neoplastic
Immunohistochemistry - veterinary
Isoenzymes - biosynthesis
Isoenzymes - genetics
Kidney - pathology
Kidney Neoplasms - enzymology
Kidney Neoplasms - genetics
Kidney Neoplasms - pathology
Kidney Neoplasms - veterinary
Male
Prostaglandin-Endoperoxide Synthases - biosynthesis
Prostaglandin-Endoperoxide Synthases - genetics
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Summary:Cyclooxygenase-2 (COX-2) has been shown to be the primary enzyme responsible for prostaglandin production during inflammation but is absent in most tissues under normal physiological states. High levels of COX-2 expression have been observed in the macula densa and thick ascending limbs of fetal kidneys; this expression declines to minimal levels during renal maturation. We hypothesized that the neoplastic cells of renal cell carcinoma (RCC) may revert to high expression of COX-2, and we evaluated its expression in three spontaneous cases of canine RCC by using immunohistochemical methods. The neoplastic cells of two of the three cases exhibited moderate to marked COX-2 immunoreactivity. These results suggest that some canine renal cell carcinomas express high levels of COX-2, which may play a role in the modulation of neoplastic cell growth.
ISSN:0300-9858
1544-2217
DOI:10.1354/vp.38-1-116