Contact information


Academic education

2003 - 2007 PhD in Theoretical Physics, University of Freiburg
1996 - 2003 Physics Studies, University of Freiburg


Scientific degrees

02/2007 PhD in Physics at the Faculty of Mathematics and Physics of the Albert-Ludwigs University Freiburg, Germany. Title: ”Concepts from Non-Linear Dynamics and Statistical Physics Applied to Complex Networks in the Life Sciences”. Graduated with summa cum laude.
02/2003 Diploma in Physics (equivalent to M.Sc.) at the Faculty of Mathematics and Physics of the Albert-Ludwigs University Freiburg, Germany. Topic: Nonparametric statistical methods applied to complex dynamical systems.


Scientific career

2018 - present Mildred-Scheel Professor on Computational Cancer Genomics (W2)
07/12    Founder of Blackfield/ New Oncology AG, acquired by Siemens Healthcare in March 2016
2013 - present Research group leader: Computational Cancer Genomics, University of Cologne
2012 - 2013   Postdoc at the Department of Translational Genomics, University of Cologne (Roman Thomas)
2008 - 2012 Postdoc at the Max-Planck Institute for Neurological Research, Cologne (Roman Thomas)
2007 - 2008 Postdoc at the Institute of Chemistry of the Karl-Franzens- University Graz, Austria (Hans-Hennig von Grünberg)
03/2007 - 04/2007 Visiting scientist at Pennsylvania State University, U.S.A., Center for Comparative Genomics and Bioinformatics (Ross Hardison and Webb Miller)


Honors/ Awards/ Memberships

2018 Mildred-Scheel Professorship of the German Cancer Aid

Member of the International Association for the Study of Lung Cancer, European Association for Cancer Research and Deutsche Physikalische Gesellschaft


  • 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.…

  • 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…

  • 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 Evolutionary History of 2,658 Cancers

    Cancer develops through a process of somatic evolution1,2. Sequencing data from a single biopsy represent a snapshot of this process that can reveal the timing of specific genomic aberrations and the changing influence of mutational processes3. Here, by whole-genome sequencing analysis of 2,658…

  • CaMuS: simultaneous fitting and de novo imputation of cancer mutational signature

    The identification of the mutational processes operating in tumour cells has implications for cancer diagnosis and therapy. These processes leave mutational patterns on the cancer genomes, which are referred to as mutational signatures. Recently, 81 mutational signatures have been inferred using…

  • 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…

  • Dissecting intratumour heterogeneity of nodal B-cell lymphomas at the transcriptional, genetic and drug-response levels

    Tumour heterogeneity encompasses both the malignant cells and their microenvironment. While heterogeneity between individual patients is known to affect the efficacy of cancer therapy, most personalized treatment approaches do not account for intratumour heterogeneity. We addressed this issue by…

  • 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…

  • 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…