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We would like to thank Dr Raspollini et al for their comments. We are excited to see that many groups have found similar results with respect to overexpression of COX-2 in epithelial ovarian cancer and the association of those changes with various markers of progression. COX-2 overexpression and its negative impact on patients' prognosis have been described in many malignancies from various primary sites. It has been shown that this protein may contribute to tumor progression through a number of pathways, including the induction of angiogenesis. In a recent publication, we demonstrated that prostaglandin E2 and hypoxia induced the expression of COX-2, vascular endothelial growth factor, and hypoxia-inducible factor 1α in epithelial ovarian cancer cells. We did find a strong correlation between COX-2 and VEGF levels, supporting the hypothesis that COX-2 does play a role in angiogenesis.1Zhu G. Saed G.M. Deppe G. Diamond M. Munkarah A.R. Hypoxia up regulates the effects of prostaglandin E2 on tumor angiogenesis in ovarian cancer cells.Gynecol Oncol. 2004; 94: 422-426Crossref PubMed Scopus (21) Google Scholar In another set of experiments using an in vitro model for angiogenesis, we showed that the COX-2 inhibitor, NS398, was able to inhibit angiogenesis induced by epithelial ovarian cancer cells. These data, added to the existing literature, support a potential role for COX-2 inhibitors in the treatment of ovarian cancer. However, this should be considered carefully in light of the recently published data on the serious adverse events associated with the use of various COX-2 inhibitors.2Solomon S.D. McMurray J.J. Pfeffer M.A. Wittes J. Fowler R. Finn P. et al.Cardiovascular risk associated with celcoxib in a clinical trial for colorectal adenoma prevention.N Engl J Med. 2005; 352: 1071-1080Crossref PubMed Scopus (1882) Google Scholar In addition, there are recent publications from independent investigators suggesting that COX-1, rather than COX-2, is the isozyme that is overexpressed in ovarian cancer and promotes angiogenesis.3Daikoku T. Wang D. Tranguch S. Morrow J.D. Orsulic S. Dubois R. et al.Cyclooxygenase-1 is a potential target for prevention and treatment of ovarian epithelial cancer.Cancer Res. 2005; 65: 3735-3744Crossref PubMed Scopus (109) Google Scholar As a result, it was suggested that COX-1 should be the potential target for treatment in this disease. We believe that it is very important to resolve this discrepancy in order to carry this line of research further and translate the laboratory findings into appropriate clinical trials. Cyclooxygenase-2, angiogenesis, tumor cell proliferation, P-glycoprotein in advanced ovarian serous carcinomaAmerican Journal of Obstetrics & GynecologyVol. 194Issue 4PreviewTo the Editors: We read with great interest the study by Ali-Fehmi et al1 regarding the role of cyclo-oxygenase-2 (COX-2) and angiogenesis in ovarian carcinoma. In a previous analysis, we investigated the COX-2 status in relation to tumor microvessel density (MVD) analyzed with the anti-CD34 monoclonal antibody, and vascular endothelial growth factor (VEGF) expression in a series of homogeneous untreated advanced serous ovarian carcinoma patients with low and high survival rate.2 In the above-mentioned study, MVD ≥70 microvessels for 200× microscopic fields was correlated with COX-2 (P = .009) and with VEGF expression (P = .003), and also, COX-2 and VEGF were correlated with one another (P = .044), according to Fisher exact test. Full-Text PDF