Genome editing in the treatment of glioblastoma

Introduction: During the past dedicates, researchers and globalexperiments about cancer of CNS and PNS, several internationalconsortia have been established to unveil the molecularbackground of human cancers including gliomas. As a result,a huge outbreak of new genetic and epigenetic data appeared.Many researchers have reported specific epigenetic features,such as DNA methylation and histone modifications being involvedin tumor pathobiology.Methods:Alterations in DNA methylation in gliomas are oneof the best described epigenetic changes underlying human pathology.GSCs are major contributors to therapy resistance in gliomas. Itwas shown that CD۱۳۳+ tumor cells, presumably GSCs, representthe cellular population unregulated alternative RNA splicing(AS). (AS) contributes to the tumorigenesis and progressionof human cancers, including glioblastoma (GBM).Major of splicing factors have been shown that serine and argininerich splicing factor ۳(SRSF۳), was frequently unregulatedin clinical glioma specimens that increase SRSF۳ was associatedwith tumor progression and a poor prognosis for patientswith glioma.miRNAs are short noncoding RNAs. miRNAs can act as oncogenesor tumor suppressors in GBM. Numerous miRNAs notonly are significant in GBM but also their expression levels canserve as diagnostic and prognostic biomarkers.Results: Cancer immunotherapy relies on getting T cells theimmune system’s primary killers of infected and diseased cellsto attack and kill tumor cells. But there’s an important stumblingblock for immunotherapy, T cells’ ability to kill can fade,a phenomenon often referred to as exhaustion.Conclusion: One sign of exhausted T cells is the increased appearanceon their surface of checkpoint proteins like PD-۱ andCTLA-۴, which can cause those T cells to stand down. Immunecheckpoint inhibitors block these checkpoint proteins and, in sodoing, can rev up the immune response against tumors