Contact information
Adaptive Immunity and Lymphoma
German Cancer Research Center (DKFZ)
Im Neuenheimer Feld 280
69120 Heidelberg
Translational and Experimental Oncology
Greifswald University Medicine
Fleischmannstraße 8
17475 Greifswald
CV
Academic education
2005 - 2009 | International Graduate School in Molecular Medicine Ulm, Ulm University |
1997 - 2004 | Medical School, Ulm University |
Scientific degrees
03/2009 | PhD, Institute of Physiological Chemistry, Ulm University. Advisor: Prof. T. Wirth (Grade: Summa cum laude) |
11/2005 | MD, Department of Internal Medicine III, Ulm University. Advisor: Prof. S. Stilgenbauer (Grade: Magna cum laude) |
Scientific career
09/2023 - present | W3 Professor in Translational and Experimental Oncology, Greifswald University Medicine |
2015 - 2023 | Max Eder research group leader at the German Cancer Research Center (DKFZ)/ National Center for Tumor Diseases (NCT) Heidelberg |
2012 - 2015 | Senior Scientist, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Immune Regulation and Cancer, Advisor: Prof. K. Rajewsky |
2009 - 2011 | Postdoctoral Fellow, Harvard Medical School, Genetics of Cancer and Immunodeficiency, Immune Disease Institute, Advisor: Prof. K. Rajewsky |
Honors/ Awards/ Memberships
2017 | Franziska Kolb Prize for Leukemia Research, University of Ulm |
2015 | Max Eder fellowship of the Deutsche Krebshilfe |
2013 | Curt Meyer Memorial Prize, Berlin Cancer Society |
2010 | Fellowship in the Career Development Program of The Leukemia & Lymphoma Society, USA |
2010 | Postdoctoral fellowship of the Deutsche Forschungsgemeinschaft (relinquished) |
2008 - present | Member of the American Association for Cancer Research |
2008 | Doctoral Student Award, International Graduate School in Molecular Medicine Ulm |
2005 | PhD student fellowship, International Graduate School in Molecular Medicine Ulm |
Publications
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Concomitant Cytotoxic Effector Differentiation of CD4+ and CD8+ T Cells in Response to EBV-Infected B Cells
Most people infected by EBV acquire specific immunity, which then controls latent infection throughout their life. Immune surveillance of EBV-infected cells by cytotoxic CD4+ T cells has been recognized; however, the molecular mechanism of generating cytotoxic effector T cells of the CD4+ subset…
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An Autochthonous Mouse Model of Myd88- and BCL2-Driven Diffuse Large B-cell Lymphoma Reveals Actionable Molecular Vulnerabilities
Based on gene expression profiles, diffuse large B-cell lymphoma (DLBCL) is subdivided into germinal center B-cell–like (GCB) and activated B-cell–like (ABC) DLBCL. Two of the most common genomic aberrations in ABC-DLBCL are mutations in MYD88 as well as BCL2 copy-number gains. Here, we employ…
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Activated gp130 signaling selectively targets B cell differentiation to induce mature lymphoma and plasmacytoma
Aberrant activity of the glycoprotein 130 130/JAK/STAT3 (gp130/JAK/STAT3) signaling axis is a recurrent event in inflammation and cancer. In particular, it is associated with a wide range of hematological malignancies, including multiple myeloma and leukemia. Novel targeted therapies have only been…
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BCR-dependent lineage plasticity in mature B cells
B2 cells engage in classical antibody responses, whereas B1 cells are considered carriers of innate immunity, biased toward recognizing epitopes present on the surfaces of common pathogens and self antigens. To explore the role of B cell antigen receptor (BCR) specificity in driving B1 cell…