TERT promoter mutations occur in the majority of glioblastoma, bladder cancer (BC), and other malignancies while the ETS family transcription factors GABPA and its partner GABPB1 activate the mutant TERT promoter and telomerase in these tumors.
GABPA depletion or the disruption of the GABPA/GABPB1 complex by knocking down GABPB1 was shown to inhibit telomerase, thereby eliminating the tumorigenic potential of glioblastoma cells.
A Radiosensitivity Gene Signature and PD-L1 Status Predict Clinical Outcome of Patients with Glioblastoma Multiforme in The Cancer Genome Atlas Dataset.
We suppose that performing a standard molecular analysis (IDH, EGFR, p53 and Ki67) is not sufficient to predict the behavior of a GBM in regards to overall survival (OS), nor to provide a deeper understanding of the meaning of the different genetic alterations in the DNA of cancer cells.
We suppose that performing a standard molecular analysis (IDH, EGFR, p53 and Ki67) is not sufficient to predict the behavior of a GBM in regards to overall survival (OS), nor to provide a deeper understanding of the meaning of the different genetic alterations in the DNA of cancer cells.
Cell Counting Kit-8 (CCK-8), wound healing, transwell assay, and flow cytometry were applied to explore the roles of DGCR5 in glioblastoma cell malignant biological behaviors.
Here, we discuss effects of the GB tumor microenvironment on NK-cell functionality, summarize early treatment attempts with <i>ex vivo</i> activated NK cells, and describe relevant CAR target antigens validated with CAR-T cells.
Here, we discuss effects of the GB tumor microenvironment on NK-cell functionality, summarize early treatment attempts with <i>ex vivo</i> activated NK cells, and describe relevant CAR target antigens validated with CAR-T cells.
Here, we discuss effects of the GB tumor microenvironment on NK-cell functionality, summarize early treatment attempts with <i>ex vivo</i> activated NK cells, and describe relevant CAR target antigens validated with CAR-T cells.
Here, we discuss effects of the GB tumor microenvironment on NK-cell functionality, summarize early treatment attempts with <i>ex vivo</i> activated NK cells, and describe relevant CAR target antigens validated with CAR-T cells.
Here, we discuss effects of the GB tumor microenvironment on NK-cell functionality, summarize early treatment attempts with <i>ex vivo</i> activated NK cells, and describe relevant CAR target antigens validated with CAR-T cells.
Here, we discuss effects of the GB tumor microenvironment on NK-cell functionality, summarize early treatment attempts with <i>ex vivo</i> activated NK cells, and describe relevant CAR target antigens validated with CAR-T cells.
Here, we discuss effects of the GB tumor microenvironment on NK-cell functionality, summarize early treatment attempts with <i>ex vivo</i> activated NK cells, and describe relevant CAR target antigens validated with CAR-T cells.
Here, we discuss effects of the GB tumor microenvironment on NK-cell functionality, summarize early treatment attempts with <i>ex vivo</i> activated NK cells, and describe relevant CAR target antigens validated with CAR-T cells.
We then outline preclinical approaches that employ CAR-NK cells for GB immunotherapy, and give an overview on the ongoing clinical development of ErbB2 (HER2)-specific CAR-NK cells currently applied in a phase I clinical trial in glioblastoma patients.
Our results indicate that anti-PD-L1 immunotherapy enhances a radiation induced abscopal response via canonical T-cell activation and direct macrophage activation in glioblastoma.
Treatment of GBM cells with MC4040 and MC4041 also impaired the GBM pro-inflammatory phenotype, with a significant decrease of TGF-β, TNF-α, and IL-6, joined to an increase of the anti-inflammatory cytokine IL-10.
Treatment of GBM cells with MC4040 and MC4041 also impaired the GBM pro-inflammatory phenotype, with a significant decrease of TGF-β, TNF-α, and IL-6, joined to an increase of the anti-inflammatory cytokine IL-10.
In conclusion, the results suggest that the recurrence of GBM is associated with high gene expression levels VEGFA and CXCL8, and the development of the central nervous system.
In conclusion, the results suggest that the recurrence of GBM is associated with high gene expression levels VEGFA and CXCL8, and the development of the central nervous system.