Klinik für Innere Medizin IIGastroenterologie, Hepatologie, Endokrinologie und Infektiologie

Research Topics

Our laboratory is focusing on a translational research approach on Barrett's Esophagus and esophageal adenocarcinoma, and the impact of gastrointestinal stem cells on inflammation induced carcinogenesis. We are working to facilitate the clinical realization of basic science principles in order to improve the care and treatment of esophagus cancer patients and the surveillance of patients with Barrett's Esophagus.

Barrett’s Esophagus (BE) is a premalignant condition of the esophagus defined by replacement of the normal squamous epithelium in the esophagus by columnar epithelium, typically with intestinal metaplasia. The development of Barrett’s esophagus represents the initial step in the histopathologic progression to low grade dysplasia, high-grade dysplasia, and esophageal adenocarinoma (EAC). The incidence of EAC, which comprises both esophageal and junctional origin, has increased at a rate of 4 to 10 % annually, an increase greater than that of any other cancer. BE and EAC are strongly associated with gastroesophageal reflux disease (GERD), and BE is present in 10 % of patients referred for GERD. GERD is thought to induce a chronic inflammatory condition of the esophagus known as reflux esophagitis, and thus chronic inflammation is thought to be one of the primary mediators of both BE and EAC. The link between inflammation and cancer is now well established, and while the mechanism is not been completely understood, it is clear that inflammatory cells release a variety of mediators that together establish an inflammatory and pro-carcinogenic microenvironment.

EAC is rapidly rising in the Western World and now accounts for at least 2 % of all cancer-related deaths, but does not develop in every patient with BE, and only over decades through progression through a sequence metaplasia to low-grade/high-grade dysplasia and carcinoma. A major limitation to the study of EAC in the past has been the absence of trackable and genetically modifyable models of BE. During my postdoc I developed the L2-IL-1b transgenic mouse model of BE and EAC. The Lab will further validate the pathogenesis of BE and EAC. Knowledge about the origin of BE and pathways driving its progression will be valuable for BE diagnosis as well as the development of novel therapies for the prevention of BE and EAC.

• BarettNET
• ColoBAC