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Contact information

Dr. med. Lukas Frenzel
Dr. med. Lukas Frenzel

Apoptosis-Signaling and Therapy Resistance Group

Department I of Internal Medicine

University Hospital of Cologne

Kerpener Straße 62 

50937 Cologne

CV

Academic education

2002 – 2008 Medical School, University of Cologne, Germany

 

Scientific degrees

03/2023 Venia legendi for Internal Medicine (habilitation), University of Cologne
09/2009 MD thesis, Institute of Neurophysiology, University of Cologne. Advisors: Prof. Dr. J. Hescheler and Dr. Dr. T. Saric; Grade: Summa cum laude
12/2008 Graduation from Medical School, (Final grade: gut), University of Cologne, Germany

 

Scientific career

2023 Co-lead Laboratory for molecular hematology and oncology (diagnostics laboratory)
10/2022 Attending physician at Department I of Internal Medicine of the University Hospital of Cologne
2019 - present Associated member of the Cologne Excellence Cluster for Aging and Aging-Associated Diseases (CECAD) 3.0
03/2019 Board examination internal medicine, hematology and oncology
2016 - present CIO (Center for Integrated Oncology) Junior group leader
2012 - present Research group leader (Apoptosis-Signaling and Therapy Resistance Group at the CECAD and Department I of Internal Medicine of the University Hospital of Cologne)
2011 - present Principal Investigator and full member of the CECAD
2011 - present Physician Scientist/ Assistant Physician
2009 - 2010 Postdoctoral Fellow University of Cologne, Advisor: Prof. Dr. C. Wendtner

 

Honors/ Awards/ Memberships

2020 Editorial board member Frontiers Oncology
2018 American Society of Hematology Abstract Achievement Award
2017  American Society of Hematology Abstract Achievement Award
2016 CIO-Roche Junior research grant
2016 Best Abstract award at the Young Investigator Meeting, IwCLL
2006 - 2008 Research stipend by the Köln Fortune Program

Publications

  • 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…

    Link to the publication

  • 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…

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  • 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.…

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  • BCL-2-family protein tBID can act as a BAX-like effector of apoptosis

    During apoptosis, the BCL-2-family protein tBID promotes mitochondrial permeabilization by activating BAX and BAK and by blocking anti-apoptotic BCL-2 members. Here, we report that tBID can also mediate mitochondrial permeabilization by itself, resulting in release of cytochrome c and mitochondrial…

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  • MARCKS affects cell motility and response to BTK inhibitors in CLL

    Bruton tyrosine kinase (BTK) inhibitors are highly active drugs for the treatment of chronic lymphocytic leukemia (CLL). To understand the response to BTK inhibitors on a molecular level, we performed (phospho)proteomic analyses under ibrutinib treatment. We identified 3466 proteins and 9184…

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  • 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…

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  • Venetoclax plus rituximab or obinutuzumab after allogeneic hematopoietic stem cell transplantation in chronic lymphocytic leukemia

    For several decades, allogeneic hematopoietic stem cell transplantation (alloHCT) has been a therapeutic option in patients with chronic lymphocytic leukemia (CLL) with high-risk features such as del(17p) and/or TP53 mutations, complex aberrant karyotype, or chemotherapy-resistant disease. With the…

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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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