A5055336567- Protein Degradation and Inhibitors
- Glioma Diagnosis and Treatment
- Multiple Myeloma Research and Treatments
- Histone Deacetylase Inhibitors Research
- Chromatin Remodeling and Cancer
- Renal and related cancers
- Barrier Structure and Function Studies
- S100 Proteins and Annexins
- Telomeres, Telomerase, and Senescence
- DNA Repair Mechanisms
- Nicotinic Acetylcholine Receptors Study
University of Fribourg
2022
University of Lausanne
2022
Weatherford College
2022
First-line drug in the treatment of glioblastoma, most severe brain cancer, is temozolomide (TMZ), a DNA-methylating agent that induces critical damage O6-methylguanine (O6MeG). This lesion cytotoxic through generation mismatch repair-mediated DNA double-strand breaks (DSBs), which trigger apoptotic pathways. Previously, we showed O6MeG also cellular senescence (CSEN). Here, show TMZ-induced CSEN late response has similar kinetics to apoptosis, but at fourfold higher level. cells high amount...
Brain metastasis is a complication of increasing incidence in patients with breast cancer at advanced disease stage. It severe condition characterized by rapid decline quality life and poor prognosis. There critical clinical need to develop effective therapies prevent treat brain metastases. Here, we describe unique robust spontaneous preclinical model the (4T1-BM 2 ) mice that has been instrumental uncovering molecular mechanisms guiding metastatic dissemination colonization brain. Key...
Abstract Bromodomain and extra-terminal tail (BET) proteins have been identified as potential epigenetic targets in cancer, including glioblastoma. These modifiers link the histone code to gene transcription that can be disrupted with small molecule BET inhibitors (BETi). With aim of developing rational combination treatments for glioblastoma, we analyzed BETi-induced differential expression glioblastoma derived-spheres, 6 distinct response patterns. To uncover emerging actionable...
Abstract Bromodomain and extra-terminal tail (BET) proteins have been identified as potential epigenetic targets in cancer, including glioblastoma. These modifiers link the histone code to gene transcription that can be disrupted with small molecule BET inhibitors (BETi). With aim of developing rational combination treatments for glioblastoma, we analyzed BETi-induced differential expression glioblastoma derived-spheres, 6 distinct response patterns. To uncover emerging actionable...
Abstract Bromodomain and extra-terminal tail (BET) proteins have been identified as potential epigenetic targets in cancer, including glioblastoma. These modifiers link the histone code to gene transcription that can be disrupted with small molecule BET inhibitors (BETi). With aim of identifying rational combination treatments for glioblastoma, we analyzed BETi-induced differential expression glioblastoma derived-spheres. This 6 distinct patterns. To uncover emerging actionable...