ABSTRACT
Colorectal cancer is common in Western countries with unanimous findings that prostaglandins are important for both carcinogenesis and progression [1-3]. It has been repeatedly observed that Cyclooxygenase-1/-2 inhibition attenuates appearance of epithelial cancer in experimental models and in part also in patients. Both primary and secondary prevention with cyclooxygenase (COX) inhibitors demonstrate and confirm decreased incidence of colorectal carcinoma in both retrospective and randomized patient cohorts [4-7]. Thus, a large number of observations emphasize that induced prostaglandin production, particularly PGE2, is involved in cell signaling through prostanoid receptors, where our own observations suggested subtype EP2 receptor expression in colon cancer tissue to predict reduced survival [2]. An important issue behind the appearance and pro-
gression of colorectal cancer seems to be increased production of PGE2 secondary to COX-2 induction in both transformed epithelial cells and host stroma [2,4,8-11]. Mechanisms behind COX-2 gene induction in colorectal cancer disease remain elusive, although a lot of information is available on the regulation of COX-2 gene expression [12,13]. Most such information has, however, been obtained in isolated cell culture experiments with obvious limitations compared to the in vivo situation based on uninterrupted host and tumor cell signaling. Therefore, the aim of the present study was to relate well-recognized external cell-and transcription factor expression to elevated tumor COX-2 expression in colorectal cancer tissue at primary operations aimed at cure.
