Abstract
Glioblastoma (GBM), a WHO-defined Grade IV astrocytoma, is the most common and aggressive CNS malignancy. Despite current treatment modalities, the survival time remains dismal. The main cause of mortality in patients with this disease is reoccurrence of the malignancy, which is attributed to treatment-resistant cancer stem cells within and surrounding the primary tumor. Inclusion of novel therapies, such as immuno- and DNA-based therapy, may provide better means of treating GBM. Furthermore, manipulation of recently discovered non-coding microRNAs, some of which regulate tumor growth through the development and maintenance of GBM stem cells, could provide new prospective therapies. Studies conducted by The Cancer Genome Atlas (TCGA) also demonstrate the role of molecular pathways, specifically the activated PI3K/AKT/mTOR pathway, in GBM tumorigenesis. Inhibition of the aforementioned pathway may provide a more direct and targeted method to GBM treatment. The combination of these treatment modalities may provide an innovative therapeutic approach for the management of GBM.
Highlights
Gliomas are tumors that arise from glial cells and are sub-classified as astrocytomas, glioblastomas, oligodendrogliomas, ependymomas, mixed gliomas, malignant gliomas not otherwise specified and Cancers 2015, 7 other rare histological variants
Motomura et al [15] analyzed 79 archival GBM samples using antibodies against 16 proteins selected according to The Cancer Genome Atlas (TCGA) classification (12,13) and identified four subcategories of GBM, namely the oligodendrocyte precursor (OPC) type, differentiated oligodendrocyte (DOC) type, astrocytic mesenchymal (AsMes) type and mixed type
The results demonstrated that both CD133+ and CD133− cells are capable of initiating proneural GBM tumors; CD133+ cells had a greater association with angiogenesis and, could lead to the formation of more aggressive tumor phenotypes [20]
Summary
Gliomas are tumors that arise from glial cells and are sub-classified as astrocytomas, glioblastomas, oligodendrogliomas, ependymomas, mixed gliomas, malignant gliomas not otherwise specified and Cancers 2015, 7 other rare histological variants. Eleven of the twelve observed mutations in IDH1 are commonly found in this class and serve as diagnostic and prognostic markers [13] Another group of tumors within the proneural subtype were found to express the glioma-CpG island methylator phenotype (G-CIMP). Motomura et al [15] analyzed 79 archival GBM samples using antibodies against 16 proteins selected according to The Cancer Genome Atlas (TCGA) classification (12,13) and identified four subcategories of GBM, namely the oligodendrocyte precursor (OPC) type, differentiated oligodendrocyte (DOC) type, astrocytic mesenchymal (AsMes) type and mixed type This histological classification confers the prognostic significance of GBM, where the OPC type with a positive IDH mutation shows a prolonged survival of 19.9 months [15]. Some of the proposed markers to be considered are mutations of IDH1, MGMT and 1p/19q co-deletion or ATRX loss, which carry significant diagnostic, prognostic and predictive abilities [16]
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