© 2002 by Oxford University Press
Journal of the National Cancer Institute, Vol. 94, No. 6, 405,
March 20, 2002
© 2002 Oxford University Press
IN THIS ISSUE |
Although the mechanisms responsible for the progression from Barretts esophagus to esophageal adenocarcinoma are unclear, it has been postulated that mucosal injury associated with gastric reflux induces the synthesis of prostaglandins and mediators of inflammation. Because cyclooxygenase (COX)-2 is the rate-limiting enzyme involved in prostaglandin synthesis, Buttar et al. (p. 422) examined the effect of inhibiting COX-2 activity in primary cultures of Barretts esophageal cells. With the use of the selective COX-2 inhibitor NS-398, the authors studied changes in the proliferation of Barretts esophageal epithelial cells. They found that inflammatory cytokines had little
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