Endocrine Abstracts

NSAIDs inhibit cyclooxygenase activity and thereby reduce prostaglandin synthesis. Two genetic isoforms of COX have been characterized: COX 1 constituvely produced in most tissues and COX 2 is not expressed in most normal tissues which is induced by pro inflammatory and mitogenic stimuli. Chronic inflammation and oxidative stress are key players in COX2 dependent carcinogenesis and it is important to point out that this type of inflammation has been associated with cancer in different tumors including endocrine tumors, such as prostate and breast cancer.

Preclinical and clinical evidence suggest that COX2 is an attractive target for the treatment or prevention of different endocrine tumors. It has been shown that COX2 is overexpressed in breast and in prostate cancer tissue.

Different mechanisms of action have been postulated: promote tumor specific angiogenesis, inhibit apoptosis, modulation of IL6, IL8 modulation of cholesterol and the final hormones (testosterone and estradiol). Also COX2 inhibitors can minimize certain typical side effects of chemotherapy such as mucositis, diarrhea and other inflammatory toxic effects.

Results from different clinical trials in will be reviewed endocrine malignancies during the meeting.