Contact information
Laboratory Tumor microenvironment and therapy resistance
Department I of Internal Medicine
University Hospital of Cologne
Kerpener Straße 62
50937 Cologne
CV
Academic education
| 1996 - 2003 | Medical School, (Final grade: Sehr gut, highest honors), University of Saarland Homburg/Saar, University of Oslo, Unversity of Cologne) |
Scientific degrees
| 2017 | Venia legendi for Internal Medicine (Habilitation), University of Cologne |
| 2015 | Board Certificate Internal Medicine, Hematology and Oncology |
| 1999 - 2003 | MD thesis, Institute for Human Genetics, University of Saarland Homburg/Saar (Grade: Summa cum laude), Advisor Prof.Dr. E. Meese, Scholar at the Graduiertenkolleg “Cellular regulation and growth” |
| 06/2004 | Graduation from Medical School, University of Cologne (Final grade: Sehr gut, highest honors) |
Scientific career
| 2019 | Professor (W2) “Tumor microenvironment and therapy resistance”, University of Cologne |
| 2018 | Attending Physician, Department I for Internal Medicine |
| 2012 - present | Research Group Leader at the Medical Clinic I of the University Hospital Cologne, CECAD Laboratories |
| 2009 - 2012 | Postdoctoral Fellow, MIT, Department of Biology, Koch Institute, Advisor: Prof. M.T. Hemann, PhD |
| 2004 - 2009 | Postdoctoral Research Fellow University of Cologne, Germany, Advisors: Prof. Dr. C.M. Wendtner and Prof. Dr. M. Hallek |
Honors/ Awards/ Memberships
| 2019 | Medical Faculty Award, best “Habilitation” in 2017 |
| 2015 | NRW-Junior Research Group Grant |
| 2010 | Research fellowship of the Deutsche Forschungsgemeinschaft |
| 2004 | “Eduard-Martin-Preis” by the University of Saarland |
| 2000 | DFG research scholarship by Graduiertenkolleg Homburg/Saar |
| 1997 | Talented Student Scholarship (Begabtenförderung) “Evangelisches Studienwerk Villigst” |
| German society for Hematology and Oncology (DGHO) | |
European Hematology Association (EHA) | |
International Society of Extracellular Vesicles (ISEV) |
Publications
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Transcriptomic profiles and 5-year results from the randomized CLL14 study of venetoclax plus obinutuzumab versus chlorambucil plus obinutuzumab in chronic lymphocytic leukemia
Data on long-term outcomes and biological drivers associated with depth of remission after BCL2 inhibition by venetoclax in the treatment of chronic lymphocytic leukemia (CLL) are limited. In this open-label parallel-group phase-3 study, 432 patients with previously untreated CLL were randomized…
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Preprint: Pentose Phosphate Pathway Inhibition activates Macrophages towards phagocytic Lymphoma Cell Clearance
Macrophages in the B-cell lymphoma microenvironment represent a functional node in progression and therapeutic response. We assessed metabolic regulation of macrophages in the context of therapeutic antibody-mediated phagocytosis. Pentose phosphate pathway (PPP) inhibition by specific compounds and…
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Deregulation and epigenetic modification of BCL2-family genes cause resistance to venetoclax in hematologic malignancies
The BCL2 inhibitor venetoclax has been approved to treat different hematological malignancies. Because there is no common genetic alteration causing resistance to venetoclax in chronic lymphocytic leukemia (CLL) and B-cell lymphoma, we asked if epigenetic events might be involved in venetoclax…
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Extracellular vesicles and PD-L1 suppress macrophages, inducing therapy resistance in TP53-deficient B-cell malignancies
Genetic alterations in the DNA damage response (DDR) pathway are a frequent mechanism of resistance to chemoimmunotherapy (CIT) in B-cell malignancies. We have previously shown that the synergy of CIT relies on secretory crosstalk elicited by chemotherapy between the tumor cells and macrophages.…
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Efficacy and Safety of Tirabrutinib and Idelalisib With or Without Obinutuzumab in Relapsed Chronic Lymphocytic Leukemia
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The scaffold protein NEDD9 is necessary for leukemia-cell migration and disease progression in a mouse model of chronic lymphocytic leukemia
The scaffold protein NEDD9 is frequently upregulated and hyperphosphorylated in cancers, and is associated with poor clinical outcome. NEDD9 promotes B-cell adhesion, migration and chemotaxis, pivotal processes for malignant development. We show that global or B-cell-specific deletion of Nedd9 in…
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Active Akt signaling triggers CLL toward Richter transformation via overactivation of Notch1
Richter's transformation (RT) is an aggressive lymphoma that occurs upon progression from chronic lymphocytic leukemia (CLL). Transformation has been associated with genetic aberrations in the CLL phase involving TP53, CDKN2A, MYC, and NOTCH1; however, a significant proportion of RT cases lack CLL…