Purpose of review
Emerging data suggest that COX-2 is involved at various steps of the process of malignant transformation and tumor progression. The current article reviews the latest data linking COX-2 with the various gynecological cancers.
COX-2 overexpression has been reported in most gynecological neoplasms, including breast, cervix, endometrial and epithelial ovarian cancers. COX-2 expression promotes tumor cell proliferation, reduces apoptosis and induces angiogenesis. As a result, tumors expressing COX-2 are reported to exhibit a more aggressive phenotype and clinical behavior. Women whose tumors over-express COX-2 tend to have a lower response to standard therapy and shorter survival times. In-vitro studies have shown that COX-2 inhibitors can inhibit tumor cell growth and reduce angiogenesis.
On the basis of the current data and the clinical availability of safe inhibitors, COX-2 is a perfect target for cancer prevention and therapy. A number of trials are investigating the benefits of combining COX-2 inhibitors with existing treatment modalities in the management of breast, ovarian and cervical cancers. In addition, large prevention trials are in the planning stage.
Abbreviations DCIS: ductal carcinoma in situ; NSAID: non-steroidal anti-inflammatory drug.