A5008229579- CAR-T cell therapy research
- Immune Cell Function and Interaction
- Lymphoma Diagnosis and Treatment
- Telomeres, Telomerase, and Senescence
- Cancer-related Molecular Pathways
- Epigenetics and DNA Methylation
- Histone Deacetylase Inhibitors Research
- Computational Drug Discovery Methods
- NF-κB Signaling Pathways
- DNA Repair Mechanisms
- Acute Lymphoblastic Leukemia research
- Immune cells in cancer
- Immunotherapy and Immune Responses
- CRISPR and Genetic Engineering
- Cytokine Signaling Pathways and Interactions
- Acute Myeloid Leukemia Research
- Cancer Research and Treatments
- Viral Infectious Diseases and Gene Expression in Insects
- Retinal and Optic Conditions
- interferon and immune responses
- Single-cell and spatial transcriptomics
- Bacterial Genetics and Biotechnology
- Cell death mechanisms and regulation
- Chronic Lymphocytic Leukemia Research
- Phagocytosis and Immune Regulation
Charité - Universitätsmedizin Berlin
2011-2025
Humboldt-Universität zu Berlin
2006-2025
Freie Universität Berlin
2018-2025
Humboldt State University
2007
Max Delbrück Center
2005
Leibniz Institute of Virology (LIV)
2002-2003
Universität Hamburg
2002-2003
University of Bremen
1998
Cellular senescence is a critical stress response program implicated in embryonic development, wound healing, aging, and immunity, it backs up apoptosis as an ultimate cell-cycle exit mechanism. In analogy to replicative exhaustion of telomere-eroded cells, premature types senescence—referring oncogene-, therapy-, or virus-induced senescence—are widely considered irreversible growth arrest states well. We discuss here that entry into full-featured not necessarily permanent endpoint, but...
In malignancies, enhanced nuclear factor-κB (NF-κB) activity is largely viewed as an oncogenic property that also confers resistance to chemotherapy. Recently, NF-κB has been postulated participate in a senescence-associated and possibly senescence-reinforcing cytokine response, thereby suggesting tumor-restraining role for NF-κB. Using mouse lymphoma model analyzing transcriptome clinical data from patients, we show here therapy-induced senescence presents with depends on active signaling,...
Transcriptional activation of p53-regulated genes is initiated by sequence-specific DNA binding p53 to target sites. Regulation complex and occurs at various levels. We demonstrate that topology an important parameter for regulating the selective highly specific interaction with its Specific wild-type greatly enhanced when cognate sites are present in a non-linear stem-loop conformation. The C-terminal domain plays key role interactions conformation-dependent manner. required conformation...
Based on gene expression profiles, diffuse large B cell lymphoma (DLBCL) is sub-divided into germinal center cell-like (GCB) and activated (ABC) DLBCL. Two of the most common genomic aberrations in ABC-DLBCL are mutations MYD88, as well BCL2 copy number gains. Here, we employ immune phenotyping, RNA-Seq whole exome sequencing to characterize a Myd88 Bcl2-driven mouse model ABC-DLBCL. We show that this resembles features human further demonstrate an actionable dependence our murine BCL2. This...
Abstract Lesion-based targeting strategies underlie cancer precision medicine. However, biological principles – such as cellular senescence remain difficult to implement in molecularly informed treatment decisions. Functional analyses syngeneic mouse models and cross-species validation patient datasets might uncover clinically relevant genetics of response programs. Here, we show that chemotherapy-exposed primary Eµ- myc transgenic lymphomas with without defined genetic lesions recapitulate...
Abstract Cellular senescence is a stress-inducible state switch relevant in aging, tumorigenesis and cancer therapy. Beyond lasting arrest, senescent cells are characterized by profound chromatin remodeling transcriptional reprogramming. We show here myeloid-skewed aberrant lineage plasticity its immunological ramifications therapy-induced (TIS) of primary human murine B-cell lymphoma. find myeloid transcription factor (TF) networks, specifically AP-1-, C/EBPβ- PU.1-governed programs,...