In the last 30 years the incidence of esophageal adenocarcinoma has greatly increased in the United States and Europe, but not in Japan. Most adenocarcinomas arise in Barrett’s esophagus, an intestinal metaplasia with goblet cells. On endoscopy in Barrett’s esophagus, the red columnar epithelium extending upwards in the lower esophagus is easily seen, and biopsies confirm metaplasia. Patients with Barrett’s esophagus usually have severe esophageal reflux, a weak lower sphincter, and hiatus hernia. Medical or surgical treatment for reflux can relieve symptoms, but the Barrett’s esophagus and increased cancer risk remain. About 5% of Barrett’s patients die from esophageal cancer. In Barrett’s, low-grade then high-grade dysplasia usually precede invasive cancer. Endoscopic biopsy surveillance of patients with Barrett’s esophagus can detect malignancy at an early, curable stage. However, most cases of Barrett’s developing adenocarcinoma are still not found until advanced cancer has developed. As about 20% of adults in the United States have reflux symptoms weekly, and 5% of these have Barrett’s esophagus, population screening for Barrett’s esophagus would be a major effort. With no, or low-grade dysplasia, surveillance endoscopy is usually done. High-grade dysplasia or early adenocarcinoma is often managed by esophagectomy; endoscopic mucosal resection for selected cases is being evaluated. Five-year survival with later-stage adenocarcinomas following transthoracic or transhiatal resection is about 15%. Controlled trials indicate surgical results may be improved by preoperative chemotherapy and radiation. For palliation of dysphagia in nonoperation cases, stent placement or endoscopic laser debulking are used.