Intestinal metaplasia in Barrett's esophagus is a major risk factor for esophageal adenocarcinoma, a tumor whose incidence rate has more than tripled in the United States over the past 2 decades. Studies have identified a number of molecular abnormalities that may be involved in the progression from dysplasia to cancer in Barrett's esophagus, including altered expression of cadherins and catenins; inactivation of tumor-suppressor genes, such as p53, p21, p27, and p16; and increased activity of the enzymes cyclooxygenase- 2 and inducible nitric oxide synthase. Studies on the role of Helicobacter pylori in the pathogenesis of intestinal metaplasia at the gastroesophageal junction have yielded contradictory results. It appears, however, that gastric infection with strains of H. pylori containing a cagA gene associated with cytotoxin expression may protect against the development of dysplasia and adenocarcinoma in Barrett's esophagus. The role of ablation therapy for Barrett's esophagus remains controversial, largely because thermal and photochemical ablative techniques often leave loci of intestinal metaplasia behind.
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