Carcinoma of the urinary bladder is the most common AQ3 malignancy in Egypt, where schistosomiasis is widespread. Cyclooxygenase-2 (COX-2), a rate-limiting enzyme in proinflammatory prostaglandin E2 biosynthesis, is up regulated in a variety of human cancers. α-Methylacyl-CoA racemase (AMACR), an enzyme involved in cellular energy metabolism by the oxidation of branched-chain fatty acids, is a biomarker that is known to be over expressed in other cancer types.
This study aims to compare/correlate the expression of COX-2 and AMACR in bladder carcinoma with/without schistosomiasis as well as assess correlation with grading and invasiveness.
Forty-six archival cases of bladder carcinoma were studied for COX-2 and AMACR immunohistochemical expression.
COX-2 was positive in 93% of cases. AMACR was positive in 26% of cases. COX-2 and AMACR positivity were significantly correlated with tumor grading. COX-2 was significantly correlated with invasion, whereas no significant relationship was found between AMACR expression and the presence or absence of invasion. No significant relationship was found between the presence or absence of schistosomiasis and both AMACR and COX-2 positivity. No significant correlation was found between positive or negative expression of COX-2 and AMACR.
It is concluded that COX-2 was found to be more frequently positive than AMACR in bladder carcinoma and its relation to inflammation may indicate its potential etiological role in bladder carcinogenesis and the lack of relation to schistosomiasis may indicate that inflammation per se may play a causative role in carcinogenesis. Association with both COX-2 and AMACR positivity and grading and the former with invasion indicate their role in tumor progression. Targeted therapy for COX-2 and AMACR may potentially be useful in the future in bladder carcinoma therapy.
Department of Pathology, Faculty of Medicine, Tanta University, Tanta, Egypt
Correspondence to Maha M. Shamloula, Department of Pathology, Faculty of Medicine, Tanta University, 3331 Tanta, Egypt Tel: +20 100 057 1583; fax: + 0020403317544; e-mail: email@example.com
Received October 24, 2011
Accepted December 9, 2011