A5051714577- Pancreatic and Hepatic Oncology Research
- Cancer Genomics and Diagnostics
- Epigenetics and DNA Methylation
- Cancer Immunotherapy and Biomarkers
- Protein Tyrosine Phosphatases
- PARP inhibition in cancer therapy
- Pancreatitis Pathology and Treatment
- Cancer, Hypoxia, and Metabolism
- Neuroendocrine Tumor Research Advances
- Cancer Cells and Metastasis
- Radiation Therapy and Dosimetry
- Cytokine Signaling Pathways and Interactions
- NF-κB Signaling Pathways
- Abdominal Trauma and Injuries
- Galectins and Cancer Biology
- Glioma Diagnosis and Treatment
- DNA Repair Mechanisms
- Immune cells in cancer
- Radiomics and Machine Learning in Medical Imaging
- Cancer-related Molecular Pathways
- Cancer Mechanisms and Therapy
- Protein Kinase Regulation and GTPase Signaling
- Phagocytosis and Immune Regulation
- Gastrointestinal Tumor Research and Treatment
- Renal cell carcinoma treatment
University Medical Center Freiburg
2016-2025
University of Freiburg
2015-2025
Technical University of Munich
2015-2025
German Cancer Research Center
2022-2024
Heidelberg University
2022-2024
Deutschen Konsortium für Translationale Krebsforschung
2024
German Marine Research Consortium
2022
Klinikum rechts der Isar
2015-2021
Center for Orthopaedics
2021
University Hospital Cologne
2014
Pancreatic ductal adenocarcinomas (PDAC) harbor recurrent functional mutations of the master DNA damage response kinase ATM, which has been shown to accelerate tumorigenesis and epithelial-mesenchymal transition. To study how ATM deficiency affects genome integrity in this setting, we evaluated molecular effects conditional Atm deletion a mouse model PDAC. was associated with increased mitotic defects, genomic rearrangements, deregulated checkpoints, reminiscent human We hypothesized that...
Over 90% of pancreatic cancers present mutations in KRAS, one the most common oncogenic drivers overall. Currently, KRAS mutant isoforms cannot be targeted directly. Moreover, targeting single RAS downstream effectors induces adaptive resistance mechanisms. We report here on combined inhibition SHP2, upstream using allosteric inhibitor RMC-4550 and ERK, LY3214996. This combination shows synergistic anti-cancer activity vitro, superior disruption MAPK pathway, increased apoptosis induction...
Encoded by PTPN11 , the Src-homology 2 domain-containing phosphatase (SHP2) integrates signals from various membrane-bound receptors such as receptor tyrosine kinases (RTKs), cytokine and integrin thereby promotes cell survival proliferation. Activating mutations in gene may trigger signaling pathways leading to development of hematological malignancies, but are rarely found solid tumors. Yet, aberrant SHP2 expression or activation has implications development, progression metastasis many...
The prognosis of pancreatic ductal adenocarcinoma (PDAC) is worse when the tumor located in body or tail, compared to being head. However, for localized, resectable tumors survival seems be at least similar. We analyzed and outcome after pancreatoduodenectomy (PD) distal pancreatectomy (DP) PDAC our institution. Clinical, pathological data from patients undergoing resection 1994–2014 were explored retrospectively, accessing a prospective database. Patients receiving primary total excluded....
ABSTRACT Pancreatic ductal adenocarcinoma remains one of the deadliest malignancies, with limited treatment options and a high recurrence rate. Recurrence happens often metastasis, for which cancer cells must adapt to isolation stress successfully colonize distant organs. While fibronectin-integrin axis has been implicated in this adaptation, its regulatory mechanisms require further elaboration. Here, we identify c-Rel as an oncogenic driver PDAC, promoting epithelial-to-mesenchymal...
Oncogenic KRAS mutations drive metabolic rewiring in pancreatic ductal adenocarcinoma (PDAC). Src-homology 2 domain-containing phosphatase (SHP2) is essential for full activity and promising dual SHP2/mitogen-activated protein kinase (MAPK) inhibition currently being tested clinical trials. Exploitable adaptations may contribute to an invariably evolving resistance. To understand the changes induced by inhibition, we comprehensively cell lines, endogenous tumor models, patient-derived...
Histone deacetylases (HDAC) catalyze N-terminal deacetylation of lysine-residues on histones and multiple nuclear cytoplasmic proteins. In various animal models, such as trauma/hemorrhagic shock, ischemic stroke or myocardial infarction, HDAC inhibitor (HDACi) application is cyto- organoprotective promotes survival. HDACi reduce stress signaling, cell death inflammation. Hepatic ischemia-reperfusion (I/R) injury during major liver resection transplantation increases morbidity mortality....
Abstract Pancreatic ductal adenocarcinoma (PDAC) is a disease with very unfavorable prognosis. Surgical resection represents the only potentially curative treatment option, but recurrence after complete almost certain. In an exploratory attempt we here aimed at identifying preoperative plasma protein biomarkers potential to predict early of PDAC. Peripheral blood samples from 14 PDAC patients divided into three groups according their time tumor curatively intended (early: < 6 months,...