In Europe and the United States, the incidence of esophageal adenocarcinoma has increased 6-fold in the last 25 years and currently accounts for more than 50% of all esophageal cancers. Barrett’s esophagus is the source of Barrett’s adenocarcinoma and is characterized by the replacement of squamous epithelium with columnar epithelium in the lower esophagus due to chronic gastroesophageal reflux disease (GERD). Even though the prevalence of GERD has recently been increasing in Japan as well as in Europe and the United States, the clinical situation of Barrett’s esophagus and Barrett’s adenocarcinoma differs from that in Western countries. In this paper, we focus on specific differences in the background factors and pathophysiology of these lesions. 1. Introduction With the increased prevalence of gastroesophageal reflux disease (GERD), the incidence of Barrett’s esophageal adenocarcinoma (BEA) derived from Barrett’s esophagus (BE) has been increasing dramatically in Europe and the United States since the 1980s and currently accounts for 60–70% of all esophageal cancers, having surpassed squamous cell carcinoma [1]. In the United States, interest in BE, the source of BEA, is high because of the explosive increase in BEA cases, despite a decrease in the overall incidence of cancer. In Japan, >90% of esophageal cancer is squamous cell carcinoma, with adenocarcinoma accounting for <1-2% [2]. However, as in Western countries, the incidence of GERD in Japan has been increasing in recent years because of Westernized eating habits and a decline in Helicobacter pylori infection in young people owing to improved hygienic environments. Therefore, even with no noticeable increase in the rate, there is a concern over the imminent increase in BEA in Japan. Nonetheless, it is currently unclear whether BEA will increase in the same fashion as it has in Europe and the United States. In this paper, we comprehensively review reports on BE and BEA and describe the current clinical situation. 2. Diagnosis of Barrett’s Esophagus The diagnosis of BE has undergone changes unique to each country since the first report by Norman Rupert Barrett in 1950. Regardless of lesion length, BE in Europe and the United States is subject to endoscopic examination followed by histological biopsy. BE is defined as a transformation of esophageal epithelium into specialized columnar epithelium including goblet cells, thus making histological examination essential in the diagnosis of BE [3]. This is particularly important because the specialized columnar epithelium is believed to play a powerful
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