<b>Objective:</b> Gliosarcoma (GSC), a rare malignant brain tumor, is considered as a variant of isocitrate dehydrogenase 1 wild type (IDH1-WT) glioblastoma (GBM).
<b>Objective:</b> Our aim is to study the prognostic value of stem cell markers (CD44, Nestin, Olig2 and SOX2) in a series of homogeneously treated GBs.
<b>Purpose:</b> HSP90, a highly conserved molecular chaperone that regulates the function of several oncogenic client proteins, is altered in glioblastoma.
<b>Purpose:</b> AZD1775, a first-in-class, small-molecule inhibitor of the Wee1 tyrosine kinase, is under evaluation as a potential chemo- and radiosensitizer for treating glioblastoma.
<b>Purpose:</b> Bevacizumab, a humanized monoclonal antibody to VEGF, is used routinely in the treatment of patients with recurrent glioblastoma (GBM).
<b>Purpose:</b> The epidermal growth factor receptor variant III (<i>EGFRvIII</i>) mutation has been considered a driver mutation and therapeutic target in glioblastoma, the most common and aggressive brain cancer.
<b>Purpose:</b> The goal of this study is to enhance the efficacy of imipridones, a novel class of AKT/ERK inhibitors that displayed limited therapeutic efficacy against glioblastoma (GBM).<b>Experimental Design:</b> Gene set enrichment, LC/MS, and extracellular flux analyses were used to determine the mechanism of action of novel imipridone compounds, ONC206 and ONC212.
<b>Result:</b> A high PRL-3 expression level was closely correlated with unfavorable OS and PFS for glioblastoma patients, and was also significantly correlated with Ki-67 expression.
<b>Results:</b> In this study, GBM cells treated with recombinant human HMGB1 (rhHMGB1) underwent spontaneous EMT through GSK-3β/Snail signaling pathway.
<b>Results:</b> We show that WNT6 is significantly overexpressed in GBMs, as compared to lower-grade gliomas and normal brain, at mRNA and protein levels.
<i>Ex vivo</i> single-cell gene expression profiling of tumors by using CD31 and α-smooth muscle actin (αSMA) as markers for endothelial cells, and pericytes and vascular smooth muscle cells (VSMCs), respectively, confirmed the predominant expression of FN, EDA+FN and EDB+FN in the vascular compartment of glioblastoma.
<i>GDF15</i> is a downstream gene of <i>S100A4</i>. miR-3189 is embedded in the intron of <i>GDF15</i>-and coexpressed with it. miR-3189-3p functions to inhibit the proliferation and migration of glioblastoma cells.
<i>In vitro</i>, miR-137 mimics inhibited GBM cell proliferation, migration and invasion, and the 3'-untranslated regions (3'-UTR) of CXCL12 were a direct target of miR-137.
<i>In vitro</i>, conditioned medium from the human glioblastoma cell line U87 activates endothelial nitric oxide synthase, causes VE-cadherin- S-nitrosylation and induces hyperpermeability.
<i>In vivo</i>, PST 3.1a reduced intersegmental vessel formation and vascularization of the subintestinal plexus in zebrafish embryos and also altered pathologic angiogenesis and glioblastoma progression <i>in vivo</i>.