A5048760213- Cancer-related Molecular Pathways
- RNA modifications and cancer
- Virus-based gene therapy research
- Cancer Research and Treatments
- Epigenetics and DNA Methylation
- MicroRNA in disease regulation
- RNA Interference and Gene Delivery
- RNA and protein synthesis mechanisms
- Cancer Cells and Metastasis
- Cancer Genomics and Diagnostics
- Thyroid Cancer Diagnosis and Treatment
- CAR-T cell therapy research
- Gene expression and cancer classification
- Bioinformatics and Genomic Networks
- DNA Repair Mechanisms
- Immunotherapy and Immune Responses
- Advanced biosensing and bioanalysis techniques
- Computational Drug Discovery Methods
- Cell death mechanisms and regulation
- Melanoma and MAPK Pathways
- Pluripotent Stem Cells Research
- CRISPR and Genetic Engineering
- Click Chemistry and Applications
- Protein Degradation and Inhibitors
- Liver physiology and pathology
University of Rostock
2016-2025
Universitätsmedizin Rostock
2015
Philipps University of Marburg
2013
Friedrich-Alexander-Universität Erlangen-Nürnberg
2013
Stellenbosch University
2013
Essen University Hospital
2004
Cancer Research UK
2004
University of Cambridge
2004
Center for Cancer Research
2004
Institute of Molecular Biology
1997-2003
Cancer is a disease of subverted regulatory pathways. In this paper, we reconstruct the network around E2F, family transcription factors whose deregulation has been associated to cancer progression, chemoresistance, invasiveness, and metastasis. We integrate gene expression profiles cell lines from two E2F1-driven highly aggressive bladder breast tumors, use analysis methods identify tumor type-specific core network. By combining logic-based modeling, in vitro experimentation, patient...
Long non-coding RNAs (lncRNAs) have emerged as integral components of E2F1-regulated gene regulatory networks (GRNs), but their implication in advanced or treatment-refractory malignancy is unknown. Methods: We combined high-throughput transcriptomic approaches with bioinformatics and structure modeling to search for lncRNAs that participate E2F1-activated prometastatic GRNs phenotypic targets the highly-relevant case E2F1-driven aggressive bladder cancer (BC). RNA immunoprecipitation was...
The p53 family member p73 displays significant structural and functional homology to p53. However, instead of mutational inactivation, overexpression wild-type has been reported in various tumor types compared with normal tissues, arguing against a classical suppressor function. Recently, N-terminally truncated, transactivation-deficient isoforms (ΔTA-p73) have identified as second class proteins. Because tumors includes ΔTA-p73, we further characterized these novel isoforms. We show that...
Stimulation of antitumor immune mechanisms is the primary goal cancer immunotherapy, and accumulating evidence suggests that effective alteration host–tumor relationship involves immunomodulating cytokines also presence costimulatory molecules. To examine effect direct in vivo gene transfer murine interleukin 12 (IL-12) B7-1 into tumors, we developed an adenovirus (Ad) vector, AdIL12–B7-1, encodes two IL-12 subunits early region 1 (E1) E3 under control cytomegalovirus promoter. This vector...
Metastases are responsible for cancer deaths, but the molecular alterations leading to tumor progression unclear. Overexpression of E2F1 transcription factor is common in high-grade tumors that associated with poor patient survival. To investigate association enhanced activity aggressive phenotype, we performed a gene-specific silencing approach metastatic melanoma model. Knockdown endogenous via small hairpin RNA (shRNA) expression increased E-cadherin SK-Mel-147 cells and reduced their...
Resistance to anti-neoplastic agents is the major cause of therapy failure, leading disease recurrence and metastasis. E2F1 a strong inducer apoptosis in response DNA damage through its capacity activate p53/p73 death pathways. Recent evidence, however, showed that E2F1, which aberrantly expressed advanced malignant melanomas together with antagonistic p73 family members, drives cancer progression. Investigating mechanisms responsible for dysregulated losing apoptotic function, we searched...
High rates of lethal outcome in tumour metastasis are associated with the acquisition invasiveness and chemoresistance.Several clinical studies indicate that E2F1 overexpression across high-grade tumours culminates unfavourable prognosis chemoresistance patients.Thus, fine-tuning expression could be a promising approach for treating patients showing chemoresistance.Methods: We integrated bioinformatics, structural kinetic modelling, experiments to study cooperative regulation by microRNA...
Angiogenesis is essential for primary tumor growth and metastatic dissemination. E2F1, frequently upregulated in advanced cancers, was recently shown to drive malignant progression. In an attempt decipher the molecular events underlying this behavior, we demonstrate that cell-associated vascular endothelial factor-C/receptor-3 (VEGF-C/VEGFR-3) axis controlled by E2F1. Activation or forced expression of E2F1 cancer cells leads upregulation VEGFR-3 its ligand VEGF-C, whereas depletion prevents...
Abstract In chronic pancreatitis ( CP ), persistent activation of pancreatic stellate cells PSC ) converts wound healing into a pathological process resulting in organ fibrosis. Here, we have analysed senescence as novel mechanism involved the termination and tissue repair. was first studied vitro by establishing long‐term cultures applying chemical triggers, using senescence‐associated β‐Galactosidase SA β‐Gal) surrogate marker. Subsequently, susceptibility to immune cell‐mediated cytolysis...
Drug resistance is a major cause of deaths from cancer. E2F1 transcription factor involved in cell proliferation, apoptosis. and metastasis through an intricate regulatory network, which includes other factors like p73 cancer-related microRNAs miR-205. To investigate the emergence drug resistance, we developed methodology that integrates experimental data with network biology kinetic modeling. Using map to summarize knowledge on its interplay p73/DNp73 miR-205 cancer responses, derived model...
Dominant-activating mutations in the RET proto-oncogene, a receptor tyrosine kinase, are responsible for development of medullary thyroid carcinoma (MTC) and causative multiple endocrine neoplasia (MEN) type 2A 2B. These tumors highly aggressive with high propensity early metastasis chemoresistance. This attribute makes this an excellent model probing mechanisms underlying cancer progression.The expression level miR-182 was measured MTC tumor specimens TT cells by real-time RT-PCR. modified...