A5025688509- Cancer-related Molecular Pathways
- Epigenetics and DNA Methylation
- Phagocytosis and Immune Regulation
- Diet and metabolism studies
- Autophagy in Disease and Therapy
- Cancer, Hypoxia, and Metabolism
- Nutrition, Genetics, and Disease
- FOXO transcription factor regulation
- Dietary Effects on Health
- Bladder and Urothelial Cancer Treatments
- Hippo pathway signaling and YAP/TAZ
- Ferroptosis and cancer prognosis
- Hepatocellular Carcinoma Treatment and Prognosis
- Cell death mechanisms and regulation
- Metabolism, Diabetes, and Cancer
- Pancreatic function and diabetes
- Cancer Research and Treatments
Comprehensive Cancer Center Vienna
2024
Medical University of Vienna
2024
Comprehensive Blood & Cancer Center
2024
U-M Rogel Cancer Center
2024
Medical University of Graz
2021-2022
University of Glasgow
2021-2022
Cancer Research UK Scotland Institute
2021-2022
Cancer Research UK
2021
Cancer cells voraciously consume nutrients to support their growth, exposing metabolic vulnerabilities that can be therapeutically exploited. Here, we show in hepatocellular carcinoma (HCC) cells, xenografts, and patient-derived organoids fasting improves sorafenib efficacy acts synergistically sensitize sorafenib-resistant HCC. Mechanistically, noncanonically as an inhibitor of mitochondrial respiration, causing resistant depend on glycolysis for survival. Fasting, through reduction glucose...
Autophagy represses YAP/TAZ-dependent hepatocyte dedifferentiation into liver progenitor cells to prevent tumorigenesis.
Purpose of review Bladder cancer incidence is on the rise, and until recently, there has been little to no change in treatment regimens over last 40 years. Hence, it imperative work strategies approaches untangle complexity intra- inter-tumour heterogeneity bladder with aim improving patient-specific care outcomes. The focus this therefore highlight novel targets, advances, therapy for patients. Recent findings success combining an antibody-drug conjugate (ADC) immunotherapy recently hailed...
The role of autophagy in cancer is complex. Both tumor-promoting and tumor-suppressive effects are reported, with tumor type, stage specific genetic lesions dictating the role. This calls for analysis models that best recapitulate each from initiation to metastatic disease, specifically understand contribution context. Here, we report deleting essential gene Atg7 a model pancreatic ductal adenocarcinoma (PDAC), which mutant Kras G12D Trp53 172H induced adult tissue leading PDAC. revealed...
Abstract Signaling trough p53is a major cellular stress response mechanism and increases upon nutrient stresses such as starvation. Here, we show in human hepatoma cell line that starvation leads to robust nuclear p53 stabilization. Using BioID, determine the cytoplasmic interaction network within immediate-early is dissociated from several metabolic enzymes kinase PAK2 for which direct binding with DNA-binding domain was confirmed NMR studies. Furthermore, proteomics after...
ABSTRACT Cancer cells voraciously consume nutrients to support their growth, exposing a metabolic vulnerability that can be therapeutically exploited. Here we show in hepatocellular carcinoma (HCC) cells, xenografts, and patient-derived HCC organoids fasting synergistically sensitize resistant sorafenib. Mechanistically, sorafenib acts non-canonically as an inhibitor of mitochondrial respiration, causing depend on glycolysis for survival. Fasting, through reduction glucose impeded...
Current standard-of-care systemic therapy options for locally advanced and metastatic bladder cancer (BC), which are predominantly based on cisplatin-gemcitabine combinations, limited by significant treatment failure rates frailty-based patient ineligibility. We previously addressed the urgent clinical need better-tolerated BC therapeutic strategies using a drug screening approach, identified outstanding antineoplastic activity of clofarabine in preclinical models BC. To further assess as...
Abstract Signaling trough p53 is a major cellular stress response mechanism and increases upon nutrient stresses such as starvation. Here, we show in human hepatoma cell line that starvation leads to robust nuclear stabilization. Using BioID, determine the cytoplasmic interaction network within immediate-early dissociated from several metabolic enzymes kinase PAK2 for which direct binding with DNA-binding domain was confirmed NMR studies. Furthermore, proteomics after immunoprecipitation...
Signaling trough p53 is a major cellular stress response mechanism and increases upon nutrient stresses such as starvation. Here, we show in human hepatoma cell line that starvation leads to robust nuclear stabilization. Using BioID, determine the cytoplasmic interaction network within immediate-early dissociated from several metabolic enzymes kinase PAK2 for which direct binding with DNA-binding domain was confirmed NMR studies. Furthermore, proteomics after immunoprecipitation (RIME)...