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GRK 1482 Jahrbuch 2011-2014

JUNIOR PRINCIPAL INVESTIGATORS Page 32 | GRK Progress Report 2011-2014 Education / Degrees 1999 - 2001 School of Medicine, Westfälische Wilhelms Universität Münster 2001 - 2004 School of Medicine, Albert-Ludwigs Universität Freiburg 2005 MD, School of Medicine, Heinrich Heine Universität, Düsseldorf 2005 Dissertation: Differential transcriptional regulation of human telomerase in a cellular model of esophageal squamous carcinogenesis Prof. Dr. Dr. H.E. Blum, Department of Medicine, University of Freiburg Positions held 2006 - 2008 Clinical Fellow, Medizinische Klinik II, Universität Bonn 2008 - 2010 Postdoctoral Fellow, Department of Digestive and Liver Disease, Columbia University Medical Center, New York 2010 - 2011 Associate Research Scientist, Columbia University Medical Center 2011 to date Clinical Fellow and Principal Investigator, II. Medizinische Klinik, Technische Universität München. Research Interests and Achievements M Quante leads a young laboratory focusing on a translational research approach on Barrett‘s Esophagus (BE) and esophageal adenocarcinoma (EAC). He is 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 gastrointestinal cancer. The correlation of chronic inflammation and obesity with or without overt infection or well-defined autoimmune processes is potential trigger of car- cinogenesis. Obesity significantly increases the risk for adenocarcinoma of the esophagus. Mechanisms by which obesity may be responsible for BE and EAC include the mechanical pathogenesis caused by increase ab- dominal obesity resulting in an increase in intragastric pressure, and the hypothesis that the hormonal, endocrine and paracrine activity of the adi- pose tissue itself might lead to contribute to an inflammatory carcinogenic phenotype. We established a mouse model, where IL-1β is over expressed in the esophageal and squamous forestomach mucosa. The mice exhibi- ted esophagitis, and with no additional intervention, the mice progressed to BE by 12 months and spontaneously to EAC as they age. Now this mouse model will be utilized to analyze the role of molecular pathways, changes to the microbiom, and role of inflammation on esophageal carcinogenesis in models of diet induced or genetic obesity Dr. Michael Quante Technische Universität München Klinikum rechts der Isar, Internal Medicine II Ismaninger Str. 22, D-81675 Munich Selected Publications Quante M, Abrams JA, Lee Y, Wang TC. Barrett Esophagus: What a mouse model can teach us about human disease. Cell Cycle. 2012 Oct 24; 11(23). QuanteM,BhagatG,AbramsJ,MaracheF,Good,P, Lee MD, Mahmood U, Lightdale C, Rustgi A, Wang TC. Bile acid and inflammation activate gastric cardia stem cells in a mouse model of Barrett’s- like metaplasia. Cancer Cell, 2012, Jan 17. Quante M, Tu S, Tomita H, Gonda T, Takashi S, Baik GH, Shibata W, Betz KS, Varro A, Tycko B, Wang TC. Bone marrow-derived myofibroblasts contribute to the mesenchymal stem cell niche and promote tumor growth. Cancer Cell, 2011 Feb 15. Research Goals Translational reseach regarding gastro intestinal carcinogenesis utilizing mouse models for gastric and esophageal cancer and human patient material and data What is the role of obesitiy with and without inflammation on gastrointestinal carcinoge- nesis and especially Barrett Esophagus How does Interleukin-1b induced inflam- mation in the esophagus or stomach influ- ence the gut microbiome