Exploring the Past, Present, and Future of Anti-Angiogenic Therapy in Glioblastoma

Glioblastoma, a WHO grade IV astrocytoma, constitutes approximately half of malignant tumors of the central nervous system. Despite technological advancements and aggressive multimodal treatment, prognosis remains dismal. The highly vascularized nature of glioblastoma enables the tumor cells to grow...

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Bibliographic Details
Published in:Cancers 2023-01, Vol.15 (3), p.830
Main Authors: Zhang, Ashley B, Mozaffari, Khashayar, Aguirre, Brian, Li, Victor, Kubba, Rohan, Desai, Nilay C, Wei, Darren, Yang, Isaac, Wadehra, Madhuri
Format: Article
Language:English
Subjects:
Angiogenesis
Angiogenesis inhibitors
Antiangiogenic agents
Astrocytoma
Bevacizumab
Blood vessels
Brain tumors
Cancer
Cancer therapies
Care and treatment
Central nervous system
Chemotherapy
Clinical trials
Development and progression
Drug therapy
Edema
FDA approval
Fibroblasts
Forecasts and trends
Glioblastoma
Glioblastoma cells
Glioblastoma multiforme
Hypertension
Hypoxia
Kinases
Medical prognosis
Monoclonal antibodies
Patients
Prognosis
Proteins
Radiation
Review
Signal transduction
Therapeutic targets
Tumor cells
Tumors
Vascular endothelial growth factor
Vascularization
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Summary:Glioblastoma, a WHO grade IV astrocytoma, constitutes approximately half of malignant tumors of the central nervous system. Despite technological advancements and aggressive multimodal treatment, prognosis remains dismal. The highly vascularized nature of glioblastoma enables the tumor cells to grow and invade the surrounding tissue, and vascular endothelial growth factor-A (VEGF-A) is a critical mediator of this process. Therefore, over the past decade, angiogenesis, and more specifically, the VEGF signaling pathway, has emerged as a therapeutic target for glioblastoma therapy. This led to the FDA approval of bevacizumab, a monoclonal antibody designed against VEGF-A, for treatment of recurrent glioblastoma. Despite the promising preclinical data and its theoretical effectiveness, bevacizumab has failed to improve patients' overall survival. Furthermore, several other anti-angiogenic agents that target the VEGF signaling pathway have also not demonstrated survival improvement. This suggests the presence of other compensatory angiogenic signaling pathways that surpass the anti-angiogenic effects of these agents and facilitate vascularization despite ongoing VEGF signaling inhibition. Herein, we review the current state of anti-angiogenic agents, discuss potential mechanisms of anti-angiogenic resistance, and suggest potential avenues to increase the efficacy of this therapeutic approach.
ISSN:2072-6694
2072-6694
DOI:10.3390/cancers15030830