A5013573948- Pancreatic and Hepatic Oncology Research
- Ubiquitin and proteasome pathways
- Immune Cell Function and Interaction
- Immune cells in cancer
- CAR-T cell therapy research
- Immunotherapy and Immune Responses
- Phagocytosis and Immune Regulation
- Global Trade and Competitiveness
- Acute Myeloid Leukemia Research
- PARP inhibition in cancer therapy
- Protein Degradation and Inhibitors
- Cell death mechanisms and regulation
Humboldt-Universität zu Berlin
2021-2023
Freie Universität Berlin
2021-2023
Max Delbrück Center
2022
Charité - Universitätsmedizin Berlin
2021-2022
Activated SUMOylation is a hallmark of cancer. Starting from targeted screening for SUMO-regulated immune evasion mechanisms, we identified an evolutionarily conserved function activated SUMOylation, which attenuated the immunogenicity tumor cells. allowed cancer cells to evade CD8+ T cell-mediated immunosurveillance by suppressing MHC class I (MHC-I) antigen-processing and presentation machinery (APM). Loss MHC-I APM frequent cause resistance immunotherapies, pharmacological inhibition...
Evasion from drug-induced apoptosis is a crucial mechanism of cancer treatment resistance. The proapoptotic protein NOXA marks an aggressive pancreatic ductal adenocarcinoma (PDAC) subtype. To identify drugs that unleash the death-inducing potential NOXA, we performed unbiased drug screening experiment. In NOXA-deficient isogenic cellular models, identified inhibitor transcription factor heterodimer CBFβ/RUNX1. By genetic gain and loss function experiments, validated mode action depends on...
Aberrant activity of the SUMOylation pathway has been associated with MYC overexpression and poor prognosis in aggressive B-cell lymphoma (BCL) other malignancies. Recently developed small-molecule inhibitors (SUMOi) target heterodimeric E1 SUMO activation complex (SAE1/UBA2). Here, we report that activated signaling is an actionable molecular vulnerability vitro a preclinical murine vivo model MYC-driven BCL. While SUMOi conferred direct effects on cells, inhibition also resulted...
One of the major challenges in cancer therapy is recurrent emergence resistance. In pancreatic cancer, we uncovered one such resistance mechanism. Inhibiting a protein which highly expressed therapy-resistant subtype could pave way for new therapies and improve survival patients.
Abstract Evasion from drug-induced apoptosis is a crucial mechanism of cancer treatment resistance. The pro-apoptotic protein NOXA marks an aggressive pancreatic ductal adenocarcinoma (PDAC) subtype. To identify drugs that unleash the death-inducing potential NOXA, we performed unbiased drug screening experiment. In -deficient isogenic cellular models identified inhibitor transcription factor heterodimer CBFβ/RUNX1. By genetic gain and loss function experiments validated mode action depends...