Relationship between COX-2 Expression, Angiogenesis and Apoptosis in Prostate Carcinoma
S Erdogan, S Zorludemir, D Gumurdulu, G Gonlusen, G Seydaoglu, B Soyupak. Cukurova University, Medical Faculty, Adana, Turkey
Background: COX is the enzyme that responsible for the production of prostaglandins from arachidonic acid. It plays role in tumorigenesis of a variety of human malignancies by stimulating cell proliferation, inhibiting epithelial differentiation, inhibiting apoptosis, mediating immune suppression. M30 is a monoclonal antibody which is used to detect the cleavage of cytokeratin 18 that occurs as an early event in epithelial cells that undergo apoptosis.The objective of this study is to determine if there is relationship between COX-2, apoptosis and angiogenesis in prostate carcinomas.
Design: COX-2, Bcl-2, VEGF and M30 were studied immunohistochemically at 49 prostate adenocarcinoma. The results of staining for COX-2, Bcl-2 and VEGF were analyzed semiquantitatively by using an immunohistochemical scoring system (HSCORE) that combines the percentage of immunoreactive cells (quantity score) and an estimate of staining intensity (staining intensity score). The number of M-30 positive cells per 1000 cells was expressed as apoptotic index.
Results: The age of the patients ranged from 48 to 73 years old (average, 63.86.4). Twenty-one (42.8%) were Gleason score 6 and 28 (57.2%) were Gleason score 7. COX-2 expression was detected in 81.6% of cases. It was significantly correlated with Bcl-2 expression (r=0.49; p<0.0001). There was no correlation between COX-2 and VEGF expression (p>0.05). Gleason score was negatively correlated with M30 (r=-0.28; p=0.04). No significant relation between Gleason score, VEGF and Bcl-2 was observed. Negative correlation between COX-2 expression and mean survival was also observed (p=0.007).
Conclusions: Our study showed an overexpression of COX-2 in prostate carcinoma. Unlike some reports, we found no relationship between COX-2 and angiogenesis (VEGF). However, COX-2 was significantly correlated with bcl-2. This raise the possibility that COX-2 may influence tumor progression in prostate carcinoma through inhibiting apoptosis rather than the promotion of angiogenesis. Selective agents targeting apoptosis and COX-2 may play role in the treatment. Additionally, expression of COX-2 is associated with a significantly worse survival. In this regard, overexpression of COX-2 may be useful for assessing the biologic behaviour of prostate carcinoma.
Category: Genitourinary (including renal tumors)
Wednesday, March 11, 2009 1:00 PM
Poster Session VI # 116, Wednesday Afternoon