Contact information

Prof. Dr. med. Christian Pallasch

Laboratory Tumor microenvironment and therapy resistance

Department I of Internal Medicine

University Hospital of Cologne

Kerpener Straße 62 

50937 Cologne


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)


  • 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…

  • 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…

  • 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…

  • 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.…

  • Efficacy and Safety of Tirabrutinib and Idelalisib With or Without Obinutuzumab in Relapsed Chronic Lymphocytic Leukemia

  • 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…

  • 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…