Expression of cyclooxygenase-2 in transitional cell carcinoma of the urinary bladder in dogs

K. Nasir M. Khan Searle Research and Development, Skokie, IL 60077.

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Deborah W. Knapp Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907-1248.

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Dennis B. Denicola Department of Veterinary Pathobiology, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907-1248.

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R. Keith Harris Searle Research and Development, Skokie, IL 60077.

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Abstract

Objective—To evaluate expression of cyclooxygenase (COX)-1 and COX-2 in the urinary bladder epithelium of clinically normal dogs and in transitional cell carcinoma cells of dogs.

Animals—21 dogs with transitional cell carcinoma of the urinary bladder and 8 dogs with clinically normal urinary bladders.

Procedure—COX-1 and COX-2 were evaluated by use of isoform-specific antibodies with standard immunohistochemical methods.

Results—COX-1, but not COX-2, was constitutively expressed in normal urinary bladder epithelium; however, COX-2 was expressed in neoplastic epithelium in primary tumors and in metastatic lesions of all 21 dogs and in new proliferating blood vessels in 3 dogs. Also, COX-1 was expressed in the neoplastic cells.

Conclusions and Clinical Relevance—Lack of expression of COX-2 in normal bladder epithelium and its substantial expression in transitional cell carcinoma cells suggest that this isoform may be involved in tumor cell growth. Inhibition of COX-2 is a likely mechanism of the antineoplastic effects of non steroidal antiinflammatory drugs. (Am J Vet Res 2000;61:478–481)

Abstract

Objective—To evaluate expression of cyclooxygenase (COX)-1 and COX-2 in the urinary bladder epithelium of clinically normal dogs and in transitional cell carcinoma cells of dogs.

Animals—21 dogs with transitional cell carcinoma of the urinary bladder and 8 dogs with clinically normal urinary bladders.

Procedure—COX-1 and COX-2 were evaluated by use of isoform-specific antibodies with standard immunohistochemical methods.

Results—COX-1, but not COX-2, was constitutively expressed in normal urinary bladder epithelium; however, COX-2 was expressed in neoplastic epithelium in primary tumors and in metastatic lesions of all 21 dogs and in new proliferating blood vessels in 3 dogs. Also, COX-1 was expressed in the neoplastic cells.

Conclusions and Clinical Relevance—Lack of expression of COX-2 in normal bladder epithelium and its substantial expression in transitional cell carcinoma cells suggest that this isoform may be involved in tumor cell growth. Inhibition of COX-2 is a likely mechanism of the antineoplastic effects of non steroidal antiinflammatory drugs. (Am J Vet Res 2000;61:478–481)

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