Contact information

Prof. Dr. med. Hans Christian Reinhardt

Department of Hematology and Stem Cell Transplantation

University Hospital Essen

Hufelandstraße 55

45147 Essen




Academic education

1996 - 2003 Medical School, University of Hamburg, Humboldt University Berlin and University of Freiburg
1999 - 2003 MD thesis, Dept. of Internal Medicine, Division 4, University of Freiburg. Entitled: Expression of functional CC- and CXC chemokine receptors in podocytes. Advisor: Prof. Dr. H. Pavenstädt (Grade: Summa cum laude)


Scientific degrees

2020- present Professor for Internal Medicine, Hematology and Stem Cell Transplantation (W3) and Director of the Clinic for Hematology and Stem Cell Transplantation, University Hospital Essen
2012 - 2020 Professor for Clinical and Molecular Oncology (W2), University Hospital Cologne
2008 Habilitation in Experimental Internal Medicine, University of Cologne
2003 MD thesis, Department of Internal Medicine, Division 4, University of Freiburg, Advisor: Prof. Dr. H. Pavenstädt (Grade: Summa cum laude)
2003 Graduation from Medical School, University of Freiburg (Grade: Summa cum laude)


Scientific career

07/2022 Co-Speaker NRW Network CANTAR - Cancer Targeting
01/2022      Vice-Speaker Collaborative Research Center "Mechanisms of Transformation and Resistance in Diffuse Large B Cell Lymphoma" (SFB-1530)
07/2020 Co-founder of CDL Therapeutics GmbH
2020 - present Professor for Internal Medicine, Hematology and Stem Cell Transplantation (W3), University Hospital Essen
2020 - present Director Dept. of Hematology and Stem Cell Transplantation, University Hospital Essen
2020 - present Elected member of the board of the Competence Network Malignant Lymphoma
2019 - present Elected member of the certification committee of the German Cancer Society (Zertifizierungskommission der Deutschen Krebsgesellschaft) for hematological malignancies
2019 - present Elected Vice-Speaker of the network of Mildred Scheel Schools of Oncology (Hamburg, Würzburg, Dresden, Frankfurt, Köln-Bonn)
2019 - present Co-Speaker Collaborative Research Center "Mechanisms of Drug Sensitivity and Resistance in Small Cell Lung Cancer" (SFB-1399)
2018 - 2020 Speaker of the Mildred Scheel School of Oncology Cologne-Bonn: Cancer- and Immuno-genomics
2017 - present Speaker of the Else Kröner Research College: Clonal evolution in cancer
2015 - 2020 Elected member of the executive board of the Center for Molecular Medicine Cologne
2013 - 2019 Head of the Clinical Research Unit-286 “Exploiting defects in the DNA damage response for the treatment of chronic lymphocytic leukemia”
2012 - 2015 Elected member of the steering committee of the Helmholtz Alliance Preclinical Comprehensive Cancer Center (PCCC) and scientific coordinator of Research Topic 3, Hematological Malignancies within the PCCC
2012 - 2020 Scientific coordinator of Research Area C (DNA damage response) within the Excellence Cluster CECAD
2012 - 2020 Professor for Clinical and Molecular Oncology (W2), University Hospital Cologne
2009 - 2015 Emmy-Noether research group leader at the Max-Planck-Institute Cologne and the Medical Clinic I of the University Hospital Cologne
2008 Habilitation for Molecular Medicine at the Medical Faculty of the University of Cologne
2004 - 2009 Postdoctoral Associate, MIT, Department of Biology, Koch Institute, Advisors: Profs. M.B. Yaffe, MD, PhD and T. Jacks, PhD
2004 Postdoctoral Research Fellow, University of Münster, Germany, Advisor: Prof. Dr. H. Pavenstädt
2003 Postdoctoral Research Fellow University of Freiburg, Germany, Advisor: Profs. Dr. G. Walz and Dr. T. Benzing


Honors/ Awards/ Memberships

2023 German Cancer Award for "Experimental Research", German Cancer Society
2021 Astra-Zeneca Scholar Award in Hematology Research
2017 Gilead Research Award Oncology
2016 Theodor Frerichs Award of the German Society of Internal Medicine
2012 GlaxoSmithKline Research Award
2011 Vincenz Czerny Award of the German Society for Hematology and Oncology
2011 W2 Lichtenberg Professorship of the Volkswagen Stiftung
2011 Research Award of the Central European Society for Anticancer Drug Research
2011 Johann-Georg-Zimmermann Award for Cancer Research
2010 Young Leaders in Science Award of the Schering Stiftung
2009 Emmy-Noether fellowship of the Deutsche Forschungsgemeinschaft
2009 Startup grant Ministerium für Innovation, Wissenschaft, Forschung und Technologie, NRW
2009 NIH/NCI K99/R00 PI award (relinquished due to return to Germany)
2007 MIT-Koch Award
2005 Research fellowship of the Deutsche Forschungsgemeinschaft
2004 Young investigator award of the Deutsche Nierenstiftung


  • 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)…

  • Noninvasive minimal residual disease assessment in relapsed/refractory large B-cell lymphoma using digital droplet PCR

    Although several promising approaches for the treatment of relapsed/refractory diffuse large B-cell lymphoma (rrDLBCL) have been approved recently, it remains unclear which patients will ultimately achieve long-term responses. Circulating tumor (ct)DNA sequencing has emerged as a valuable tool to…

  • Mouse models of diffuse large B cell lymphoma

    Diffuse large B cell lymphoma (DLBCL) is a genetically highly heterogeneous disease. Yet, to date, the vast majority of patients receive standardized frontline chemo-immune-therapy consisting of an anthracycline backbone. Using these regimens, approximately 65% of patients can be cured, whereas the…

  • 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…

  • Entirely noninvasive outcome prediction in central nervous system lymphomas using circulating tumor DNA

    State-of-the-art response assessment of central nervous system lymphoma (CNSL) by magnetic resonance imaging is challenging and an insufficient predictor of treatment outcomes. Accordingly, the development of novel risk stratification strategies in CNSL is a high unmet medical need. We applied…

  • CDK9 inhibition as an effective therapy for small cell lung cancer

    Treatment-naïve small cell lung cancer (SCLC) is typically susceptible to standard-of-care chemotherapy consisting of cisplatin andetoposide recently combined with PD-L1 inhibitors. Yet, in most cases, SCLC patients develop resistance to first-line therapy andalternative therapies are urgently…

  • 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.…

  • Outcome Prediction in Patients With Large B-cell Lymphoma Undergoing Chimeric Antigen Receptor T-cell Therapy

    The introduction of chimeric antigen receptor (CAR) T-cell therapy has led to a fundamental shift in the management of relapsed and refractory large B-cell lymphoma. However, our understanding of risk factors associated with non-response is still insufficient and the search for predictive biomarkers…

  • 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…

  • Interim FDG-PET analysis to identify patients with aggressive non-Hodgkin lymphoma who benefit from treatment intensification: a post-hoc analysis of the PETAL trial

    The randomized PETAL trial failed to demonstrate a benefit of interim FDG-PET (iPET)-based treatment intensification over continued standard therapy with CHOP (plus rituximab (R) in CD20-positive lymphomas). We hypothesized that PET analysis of all lymphoma manifestations may identify patients who…

  • 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…

  • Ferroptosis response segregates small cell lung cancer (SCLC) neuroendocrine subtypes

    Loss of TP53 and RB1 in treatment-naïve small cell lung cancer (SCLC) suggests selective pressure to inactivate cell death pathways prior to therapy. Yet, which of these pathways remain available in treatment-naïve SCLC is unknown. Here, through systemic analysis of cell death pathway availability…

  • Meta-Analysis Reveals Significant Sex Differences in Chronic Lymphocytic Leukemia Progression in the Eµ-TCL1 Transgenic Mouse Model

    The Eµ-TCL1 transgenic mouse model represents the most widely and extensively used animal model for chronic lymphocytic leukemia (CLL). In this report, we performed a meta-analysis of leukemia progression in over 300 individual Eµ-TCL1 transgenic mice and discovered a significantly accelerated…

  • 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…

  • Altered DNA Methylation Profiles in SF3B1 Mutated CLL Patients

    Mutations in splicing factor genes have a severe impact on the survival of cancer patients. Splicing factor 3b subunit 1 (SF3B1) is one of the most frequently mutated genes in chronic lymphocytic leukemia (CLL); patients carrying these mutations have a poor prognosis. Since the splicing machinery…

  • 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…

  • 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…

  • Aberrant expansion of spontaneous splenic germinal centers induced by hallmark genetic lesions of aggressive lymphoma

    Unique molecular vulnerabilities have been identified in the aggressive MCD/C5 genetic subclass of diffuse large B-cell lymphoma (DLBCL). However, the premalignant cell-of-origin exhibiting MCD-like dependencies remains elusive. In this study, we examined animals carrying up to 4 hallmark genetic…