Publications by authors named "Anna Koessinger"
Background: Glioblastomas have highly infiltrative growth patterns that contribute to recurrence and poor survival. Despite infiltration being a critical therapeutic target, no clinically useful therapies exist that counter glioblastoma invasion. Here, we report that inhibition of ataxia telangiectasia and Rad 3 related kinase (ATR) reduces invasion of glioblastoma cells through dysregulation of cytoskeletal networks and subsequent integrin trafficking.
View Article and Find Full Text PDFGlomerular disease due to podocyte malfunction is a major factor in the pathogenesis of chronic kidney disease. Identification of podocyte-specific signaling pathways is therefore a prerequisite to characterizing relevant disease pathways and developing novel treatment approaches. Here, we employed loss of function studies for () as a central podocyte gene to generate a cell type-specific disease model.
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- Scientists studied how glioblastoma (GBM), a type of brain cancer, spreads in the brain and why it keeps coming back after treatment.
- They looked at tiny particles called extracellular vesicles (EVs) that GBM cells release and how these particles help the cancer invade the brain.
- The research found that a mutant gene in GBM makes these EVs, which cause certain brain cells (astrocytes) to create a supportive environment for the cancer to grow and move, making it harder to stop the disease.
Glioblastoma (GBM) is the most prevalent malignant primary brain tumour in adults. GBM typically has a poor prognosis, mainly due to a lack of effective treatment options leading to tumour persistence or recurrence. We investigated the therapeutic potential of targeting anti-apoptotic BCL-2 proteins in GBM.
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- Apoptosis is when damaged cells die, but some of these dying cells help nearby healthy cells survive by sending signals.* -
- They release a special growth factor called FGF2, which helps the nearby cells create protective proteins called BCL-2 that keep them alive.* -
- In certain cancers, this signal can make the cancer worse, but it also plays a part in how our skin heals after it gets hurt.*
Article Synopsis
- Little progress in glioblastoma therapy is attributed to inadequate preclinical in vivo models, leading to the use of primary patient-derived cell lines that maintain stem-like characteristics.
- Due to the heterogeneous nature of glioblastoma, larger experimental groups are often needed for studies using these primary cells, making imaging techniques essential for monitoring tumor growth.
- The study demonstrates that equipping patient-derived glioblastoma cells with a near-infrared fluorescent protein (iRFP) allows for effective, non-invasive monitoring of tumor development, enhancing quantitative evaluation of tumor burden without introducing variability from agents like luciferin.
Purpose: The incidence of mesothelioma continues to rise and prognosis remains dismal owing to resistance to conventional therapies and few novel treatment options. Failure to activate apoptotic cell death is a resistance mechanism that may be overcome by inhibition of antiapoptotic Bcl-2 proteins using BH3-mimetic drugs. We investigated the role of antiapoptotic proteins in the radioresistance of mesothelioma, identifying clinically relevant targets for radiosensitization and evaluating the activity of BH3-mimetics alone and in combination with radiation therapy in preclinical models.
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