Contact information


Academic education

1991 - 1998 Resident of Pathology and Staff Pathologist, Regensburg
1986 - 1987 Resident of Pathology, RWTH Aachen
1979 - 1985 Studies of Human Medicine, Mainz, Munich, London (UK), Cologne


Scientific degrees

1996 Habilitation (University of Regensburg)
1986 MD thesis (LMU Munich)


Scientific career

2011 - present Professor and Chairman for Pathology, University of Cologne
2007 - 2009 Dean of the Medical Faculty, University of Bonn
2001 - 2011 Professor and Chairman for Pathology, University of Bonn
1999 - 2001 Full Professor for Pathology (C3), RWTH Aachen
1987 - 1990 Postdoctoral research fellow Gene Center Munich and MD Anderson Cancer Center, Houston (TX), DFG Fellowship


Honors/ Awards/ Memberships

2024 President of the German Cancer Congress, Berlin
2023 Co-Founder and co-owner of Timer Therapeutixs Inc.
2022 Co-Founder of Gnothis Inc, Stockholm
2020 PI and Applicant for the National Center of Tumor Diseases Cologne/Essen
2019 Member of the Board of Trustees of the LNS, Luxembourg
2018 - 2020  Speaker of EFRE Project “ImmunePredict”
2018 - present Speaker of national Network Genomic Medicine (nNGM
2016 Member of the Board of Trustees of the German Cancer Aid
2016 Co-Organizer of the Joint IAP/ESP World Pathology Conference/Cologne
2015 Founding President of the Vladimir Totovic Foundation/German Pathology
2011 - 2012 President of the German Division of the International Academy of Pathology
2009 - present Member of the German Academy for Sciences (Leopoldina), Academia Moguntia and the Academy for Sciences NRW
2009 Executive Board Member, Mildred Scheel Foundation for Cancer Research
2008 - 2012 Speaker of the German Sarcoma Group KoSAR funded by the German Cancer Aid
2006 Co-founder and co-owner of Targos Molecular Diagnostics GmbH
1997 - 2000 Speaker of the DFG Collaborative Research Group “Programmed Cell Death in Neuronal Systems”
1979 - 1985 Stipend from the German National Scholarship Foundation


  • 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…

  • LYN kinase programs stromal fibroblasts to facilitate leukemic survival via regulation of c-JUN and THBS1

    Microenvironmental bystander cells are essential for the progression of chronic lymphocytic leukemia (CLL). We have discovered previously that LYN kinase promotes the formation of a microenvironmental niche for CLL. Here we provide mechanistic evidence that LYN regulates the polarization of stromal…

  • The X-linked trichothiodystrophy-causing gene RNF113A links the spliceosome to cell survival upon DNA damage

    Prolonged cell survival occurs through the expression of specific protein isoforms generated by alternate splicing of mRNA precursors in cancer cells. How alternate splicing regulates tumor development and resistance to targeted therapies in cancer remain poorly understood. Here we show that…

  • 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…

  • 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…

  • Tripartite antigen-agnostic combination immunotherapy cures established poorly immunogenic tumors

    Single-agent immunotherapy has shown remarkable efficacy in selected cancer entities and individual patients. However, most patients fail to respond. This is likely due to diverse immunosuppressive mechanisms acting in a concerted way to suppress the host anti-tumor immune response. Combination…

  • Pericentromeric Satellite III transcripts induce etoposide resistance

    Non-coding RNA from pericentromeric satellite repeats are involved in stress-dependent splicing processes, maintenance of heterochromatin, and are required to protect genome stability. Here we show that the long non-coding satellite III RNA (SatIII) generates resistance against the topoisomerase IIa…

  • Inhibition of Tumor VEGFR2 Induces Serine 897 EphA2-Dependent Tumor Cell Invasion and Metastasis in NSCLC

    Anti-angiogenic treatment targeting vascular endothelial growth factor (VEGF)-VEGFR2 signaling has shown limited efficacy in lung cancer patients. Here, we demonstrate that inhibition of VEGFR2 in tumor cells, expressed in ∼20% of non-squamous non-small cell lung cancer (NSCLC) patients, leads to a…

  • Integrative Analysis of Pleomorphic Dermal Sarcomas Reveals Fibroblastic Differentiation and Susceptibility to Immunotherapy

    Pleomorphic dermal sarcoma (PDS) is a rare malignant cutaneous tumor with an unknown cell of origin. Locally defined tumors can be treated by curative excisions, whereas advanced stages of the disease are difficult to treat, using standard regimens. We performed whole-exome sequencing on a cohort…

  • 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…

  • 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…

  • 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…