Publications by authors named "Costanza Lo Cascio"
Histone deacetylase (HDAC) inhibitors have garnered considerable interest for the treatment of adult and pediatric malignant brain tumors. However, owing to their broad-spectrum nature and inability to effectively penetrate the blood-brain barrier, HDAC inhibitors have failed to provide substantial clinical benefit to patients with glioblastoma (GBM) to date. Moreover, global inhibition of HDACs results in widespread toxicity, highlighting the need for selective isoform targeting.
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- The perivascular niche (PVN) is a key area in glioblastoma that helps glioma stem cells (GSCs) survive and promote tumor recurrence, making understanding its cellular interactions important for creating effective treatments.
- Research has revealed limitations in current models for studying the PVN, prompting the development of a new organotypic triculture microfluidic model that includes endothelial cells (ECs), astrocytes, and GSCs to better investigate their interactions.
- The study found that ECs and astrocytes enhance GSC invasiveness and identified 15 significant ligand-receptor pairs, including the SAA1-FPR1 pair, which could be targets for new therapeutic approaches in treating glioblastoma.
Glioblastoma (GBM) is characterized by an aberrant yet druggable epigenetic landscape. One major family of epigenetic regulators, the histone deacetylases (HDACs), are considered promising therapeutic targets for GBM due to their repressive influences on transcription. Although HDACs share redundant functions and common substrates, the unique isoform-specific roles of different HDACs in GBM remain unclear.
View Article and Find Full Text PDFMalignant gliomas are the most common, infiltrative, and lethal primary brain tumors affecting the adult population. The grim prognosis for this disease is due to a combination of the presence of highly invasive tumor cells that escape surgical resection and the presence of a population of therapy-resistant cancer stem cells found within these tumors. Several studies suggest that glioma cells have cleverly hijacked the normal developmental program of neural progenitor cells, including their transcriptional programs, to enhance gliomagenesis.
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- In glioblastoma, there's a crucial link between the phosphorylation state of the transcription factor OLIG2 and the tumor cells' ability to switch between growth and invasion.
- Unphosphorylated OLIG2 enhances cell migration and invasion by increasing TGF-β2 expression, while phosphorylated OLIG2 prevents this invasive behavior.
- Targeting the TGF-β2 pathway could be a potential strategy for treating glioblastoma by limiting the invasive capabilities of tumor cells.