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The rapid rise in gastroesophageal junction tumors: is inflammation of the gastric cardia the underwater iceberg?

Over the last 40 years, there has been a rapid rise in the incidence of esophageal adenocarcinoma (EAC) as well as proximal gastric cardia adenocarcinoma (GCC, also known as junctional adenocarcinoma). Although most of the focus has been on EAC, which has been strongly linked to Barrett’s esophagus (BE), GCCs arise in a contiguous location at the squamocolumnar junction (SCJ), and are often difficult to distinguish from EAC at a clinical or pathologic level. Furthermore, whereas gastroesophageal reflux and BE are clearly defined risk factors for EAC, most patients with EAC do not have a strong history of reflux, and EAC lesions show surrounding or associated specialized BE mucosa in fewer than half of cases. Recent publications have raised the question of whether EAC and GCC might possibly arise from the same origin and should therefore be described as one entity.1–4 Moreover, in the clinical setting, screening and surveillance of at-risk patients has been limited to individuals with BE with intestinal metaplasia (IM), and this strategy is unlikely to impact the overall incidence of EAC/GCC. It remains unclear as to whether any patients without reflux symptoms should be considered for screening. In addition, no efforts have been made to identify patients at risk for GCC, in part because risk factors and markers for GCC are poorly described.