Contact information
Department I of Internal Medicine
University Hospital of Cologne
TRIO
University of Cologne
Robert-Koch-Straße 21
50931 Cologne
CV
Academic education
| 2010 - 2016 | Medical School, University of Bonn, Germany |
Scientific degrees
| 2016 | Doctoral Thesis at the Institute of Molecular Medicine, Medical Faculty of the University of Bonn, Germany, supervisor: Prof. Veit Hornung, and the École polytechnique fédérale de Lausanne (EPFL), Lausanne, Switzerland, supervisor: Prof. Andrea Ablasser |
Scientific career
| 2025 - present | Junior Group Leader, Department I of Internal Medicine, University Hospital Cologne, Germany |
| 2021 - 2024 | Guest Scientist / Postdoctoral Fellow, Max-Planck-Institute for Biology of Ageing, Cologne, Germany |
| 2017 - 2021 | Postdoctoral Fellow, Department I of Internal Medicine, University Hospital Cologne, Germany |
| 2016 - present | Resident Physician, Department I of Internal Medicine, University Hospital Cologne, Germany |
| 2015 - 2016 | Resident Physician, Department III of Internal Medicine, Oncology and Hematology, University Hospital Bonn, Germany |
| 2014 | Doctoral assistant at the École polytechnique fédérale de Lausanne (EPFL), Lausanne, Switzerland |
Honors/ Awards/ Memberships
| 2024 - present | Member of the German Society of internal Medicine (DGIM) |
| 2024 - present | Member of the German Lymphoma Alliance (GLA) |
Publications
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An inducible Cd79b mutation confers ibrutinib sensitivity in mouse models of Myd88-driven diffuse large B-cell lymphoma
- In mouse models of Myd88-driven DLBCL, the presence of a Cd79b ITAM mutation results in increased BCR proximal signaling. - The increased BCR signaling activity in Cd79b-mutated models confers a selective ibrutinib sensitivity. Diffuse large B cell lymphoma (DLBCL) is the most common…
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An anti-CD19/CTLA-4 switch improves efficacy and selectivity of CAR T cells targeting CD80/86-upregulated DLBCL
himeric antigen receptor T cell (CAR T) therapy is a potent treatment for relapsed/refractory (r/r) B cell lymphomas but provides lasting remissions in only ∼40% of patients and is associated with serious adverse events. We identify an upregulation of CD80 and/or CD86 in tumor tissue of (r/r)…
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An Aged/Autoimmune B-cell Program Defines the Early Transformation of Extranodal Lymphomas
A third of patients with diffuse large B-cell lymphoma (DLBCL) present with extranodal dissemination, which is associated with inferior clinical outcomes. MYD88L265P is a hallmark extranodal DLBCL mutation that supports lymphoma proliferation. Yet extranodal lymphomagenesis and the role of…
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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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CSF1R+ myeloid-monocytic cells drive CAR-T cell resistance in aggressive B cell lymphoma
Despite the improvement, approximately 60% of patients with relapsed or refractory (r/r) aggressive B cell lymphoma (B-NHL) do not achieve durable benefit from CAR-T cell therapy. To elucidate factors associated with CAR-T therapy resistance, we conducted high-dimensional analyses of pre- and…
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Distinct Genetically Determined Origins of Myd88/BCL2-Driven Aggressive Lymphoma Rationalize Targeted Therapeutic Intervention Strategies
Genomic profiling revealed the identity of at least 5 subtypes of diffuse large B-cell lymphoma (DLBCL), including the MCD/C5 cluster characterized by aberrations in MYD88, BCL2, PRDM1, and/or SPIB. We generated mouse models harboring B cell–specific Prdm1 or Spib aberrations on the background of…