Current Opportunities for Targeting Dysregulated Neurodevelopmental Signaling Pathways in Glioblastoma

Glioblastoma (GBM) is the most common and highly lethal type of brain tumor, with poor survival despite advances in understanding its complexity. After current standard therapeutic treatment, including tumor resection, radiotherapy and concomitant chemotherapy with temozolomide, the median overall s...

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Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2022-08, Vol.11 (16), p.2530
Main Authors: Drakulic, Danijela, Schwirtlich, Marija, Petrovic, Isidora, Mojsin, Marija, Milivojevic, Milena, Kovacevic-Grujicic, Natasa, Stevanovic, Milena
Format: Article
Language:English
Subjects:
Brain cancer
Brain tumors
Cell cycle
Cellular signal transduction
Chemotherapy
DNA methylation
Drug targeting
Drug therapy
GBM subtypes
Gene expression
Glioblastoma
Glioblastoma multiforme
Health aspects
Hypoxia
Medical prognosis
Methods
Mutation
Neurons
Notch signaling
Radiation therapy
Review
SHH signaling
Signal transduction
Stem cells
Temozolomide
TGFβ signaling
Tumors
Wnt/β-catenin signaling
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Summary:Glioblastoma (GBM) is the most common and highly lethal type of brain tumor, with poor survival despite advances in understanding its complexity. After current standard therapeutic treatment, including tumor resection, radiotherapy and concomitant chemotherapy with temozolomide, the median overall survival of patients with this type of tumor is less than 15 months. Thus, there is an urgent need for new insights into GBM molecular characteristics and progress in targeted therapy in order to improve clinical outcomes. The literature data revealed that a number of different signaling pathways are dysregulated in GBM. In this review, we intended to summarize and discuss current literature data and therapeutic modalities focused on targeting dysregulated signaling pathways in GBM. A better understanding of opportunities for targeting signaling pathways that influences malignant behavior of GBM cells might open the way for the development of novel GBM-targeted therapies.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells11162530