Abstract and Introduction
Angiogenesis is a central feature of glioblastoma (GBM), with contribution from several mechanisms and signaling pathways to produce an irregular, poorly constructed, and poorly connected tumor vasculature. Targeting angiogenesis has been efficacious for disease control in other cancers, and given the (I) highly vascularized environment in GBM and (II) correlation between glioma grade and prognosis, angiogenesis became a prime target of therapy in GBM as well. Here, we discuss the therapies developed to target these pathways including vascular endothelial growth factor (VEGF) signaling, mechanisms of tumor resistance to these drugs in the context of disease progression, and the evolving role of anti-angiogenic therapy in GBM.
Glioblastoma (GBM) is the most aggressive and unfortunately most common, malignant primary brain tumor, with a median survival of 10–31 months depending on age at diagnosis, extent of resection, treatment and molecular prognostic factors.[1–4] Angiogenesis is a central feature of GBM, with microvascular glomeruloid proliferation requisite for histological diagnosis.[5,6] Endothelial cells comprise the tumor blood vessels, facilitating delivery of nutrients and oxygen. In addition, endothelial cells directly support glioma progenitor cell proliferation through intercellular signaling pathways, contributing to tumor growth and resilience.
Chin Clin Oncol. 2021;10(4):37 © 2021 AME Publishing Company