Abstract
Glioblastoma (GBM) is aggressive malignant tumor residing within the central nervous system. Although the standard treatment options, consisting of surgical resection followed by combined radiochemotherapy, have long been established for patients with GBM, the prognosis is still poor. Despite recent advances in diagnosis, surgical techniques, and therapeutic approaches, the increased patient survival after such interventions is still sub-optimal. The unique characteristics of GBM, including highly infiltrative nature, hard-to-access location (mainly due to the existence of the blood brain barrier), frequent and rapid recurrence, and multiple drug resistance mechanisms, pose challenges to the development of an effective treatment. To overcome current limitations on GBM therapy and devise ideal therapeutic strategies, efforts should focus on an improved molecular understanding of GBM pathogenesis. In this review, we summarize the molecular basis for the development and progression of GBM as well as some emerging therapeutic approaches.
Highlights
Glioblastoma (GBM), often referred to as a grade IV astrocytoma, is an aggressive malignant tumor that occurs in the brain or spinal cord
We summarize the current knowledge of molecular therapeutic approaches pathogenesis and the for current/emerging therapeutic approaches for GBM
Isocitrate dehydrogenase (IDH) mutations result in hypermethylation of a subset of CTCF (CCCTC-binding factor) binding sites leading to a significant alteration in the three-dimensional structure of DNA [48]
Summary
Glioblastoma (GBM), often referred to as a grade IV astrocytoma, is an aggressive malignant tumor that occurs in the brain or spinal cord. Owing to the unique location of GBM, drugs should penetrate the blood brain barrier (BBB) to reach the tumor site. The main feature of the classical subtype is a high-level EGFR gene amplification and class presents a lower NF1 expression. Each subtype shows different clinical characteristics the mesenchymal class presents a lower NF1 expression. To overcome the current limitation on GBM treatment and develop ideal clinical characteristics and treatment efficacy [9]. To overcome the current limitation on GBM personalized therapies, improved molecular understanding of GBM pathogenesis is essential. 1. Relative gene expressions in four subtypes of GBM. Relative mRNA expressions (left) and (left)mean and difference p valuespbetween each subtype (right) (right) of EGFR (A), IDH1.
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