| dc.description.abstract | Glioblastoma Multiforme (GBM) is a potent type of cancer due to its high mortality and aggressive nature with a median survival of 14 months post-diagnosis (1, 2). Immunotherapies are a promising approach to treating GBMs by remodeling the tumor microenvironment to recruit T cells and natural killer (NK) cells (3). Radiation therapy is known to increase tumor immunogenicity through increased T-cell infiltration stimulated by type I interferon (IFN) production, which is triggered by various cell-signaling pathways such as cGAS-STING and RIG-1 (4). However, the relative contribution of each of these pathways toward the IFN response is not well understood, which limits the ability to harness a robust immune anti-tumor response. This research suggests that the occurrence of STING activation in GBM cells subsequent to radiation treatment, leads to the generation of immune-stimulating cytokines, albeit with variable degrees of activation. These findings substantiate the potential of employing STING pathway modulators as a promising component of therapies targeting GBM. | en_US |
