Pathogenese und Prävention von ösophagealen Adenokarzinomen

Esophageal adenocarcinoma (EAC) has the most rapidly increasing incidence rate of all tumor diseases in industrialized countries. For efficient healthcare, it is essential that the reasons for this are understood. The most important known premalignant precursor is Barrett’s esophagus (BE). Until now, BE has been mainly attributed to inflammation due to chronic reflux. A new preclinical mouse model and current studies in humans suggest that EAC arises not in the esophagus, but in the stomach’s cardia. Attracted by the inflammatory microenvironment, stem cells from the cardia expand into the esophagus and promote carcinogenesis. Results show that these stem cells are activated by alteration of the inflammatory microenvironment in the esophagus, which is presumably influenced by multiple factors such as age, gender, and obesity etc., alongside genetic and molecular changes. Identification of these factors is necessary for optimization of risk stratification and establishment of prevention strategies. The main aim is to identify biomarkers which enable early classification of high-risk patients in order to offer an efficient and risk-adapted surveillance program, thus minimizing the number of surveillance endoscopies. This would decrease costs and effort, and provide better care for the individual patient. Despite promising approaches, no clinically practicable biomarker sets capable of reaching this goal are available as yet. Future research on better biomarkers for the malignant progression of BE is therefore of substantial importance.