<b>Abbreviations</b>: AAAIR: Average Annual Age-Adjusted Incidence Rate; AI/AN: American Indian or Alaska Native; API: Asian or Pacific Islander; CBTRUS: Central Brain Tumor Registry of the United States; CUMC: Columbia University Medical Center; EOR: Extent of Resection; Exc: Excluded; GBM: Glioblastoma; GTR: Gross Total Resection; IDH-1: Isocitrate Dehydrogenase 1; MGMT: O6-Methylguanine DNA Methyltransferase; NCDB: National Cancer Database; OS: Overall Survival; O/U: Other/Unknown; PFS: Progression-Free Survival; SEER: Surveillance, Epidemiology, and End Results; S&W BTR: Scott & White Brain Tumor Registry; UCLA: University of California Los Angeles; UM: University of Miami.
<b>Background:</b> Wnt5a is a nontransforming Wnt family member and identified as an oncogenic role on cell motility of breast cancer and glioblastoma.
<b>Conclusion:</b> High radiation doses to ipsilateral NSC and contralateral SVZ could have a negative impact on overall survival in IDH-wild-type glioblastoma population.
<b>Conclusion:</b> High radiation doses to ipsilateral NSC and contralateral SVZ could have a negative impact on overall survival in IDH-wild-type glioblastoma population.
<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> 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>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.
<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>, 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>.
<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>.
<i>NEAT1</i> depletion also inhibited GBM cell growth and invasion in the intracranial animal model.<b>Conclusions:</b> The EGFR/<i>NEAT1</i>/EZH2/β-catenin axis serves as a critical effector of tumorigenesis and progression, suggesting new therapeutic directions in glioblastoma.<i></i>.
<sup>18</sup>F-GE-180, a novel TSPO ligand, has shown improved binding affinity and a high target-to-background contrast in patients with glioblastoma.