Glioblastoma (GBM) is associated with a high degree of angiogenesis. Therefore, antiangiogenic therapy could have a role in the treatment of this tumor. The currently available treatment approaches acting against angiogenesis are mainly directed toward three pathways: VEGF pathway, VEGF-independent pathways and inhibition of vascular endothelial cell migration. It has been demonstrated that antiangiogenic therapy can produce a rapid radiological response and a decrease of brain edema, without significantly influencing survival. Future studies should consider that: animal models are inadequate and cells used for animal models (mainly U87) are deeply different from patient GBM cells; GBM cells may become resistant to antiangiogenic therapy and some cells may be resistant to antiangiogenic therapy ab initio; and angiogenesis in the peritumor tissue has been poorly investigated. Therefore, the ideal target of angiogenesis is probably yet to be identified.
De Bonis, P., Marziali, G., Vigo, V., Peraio, S., Pompucci, A., Anile, C., Mangiola, A., Antiangiogenic therapy for high-grade gliomas: current concepts and limitations, <<EXPERT REVIEW NEUROTHERAPEUTICS>>, 2013; 13 (11): 1263-1270. [doi:10.1586/14737175.2013.856264] [http://hdl.handle.net/10807/53888]
Antiangiogenic therapy for high-grade gliomas: current concepts and limitations
De Bonis, Pasquale;Vigo, Vera;Peraio, Simone;Pompucci, Angelo;Anile, Carmelo;Mangiola, Annunziato
2013
Abstract
Glioblastoma (GBM) is associated with a high degree of angiogenesis. Therefore, antiangiogenic therapy could have a role in the treatment of this tumor. The currently available treatment approaches acting against angiogenesis are mainly directed toward three pathways: VEGF pathway, VEGF-independent pathways and inhibition of vascular endothelial cell migration. It has been demonstrated that antiangiogenic therapy can produce a rapid radiological response and a decrease of brain edema, without significantly influencing survival. Future studies should consider that: animal models are inadequate and cells used for animal models (mainly U87) are deeply different from patient GBM cells; GBM cells may become resistant to antiangiogenic therapy and some cells may be resistant to antiangiogenic therapy ab initio; and angiogenesis in the peritumor tissue has been poorly investigated. Therefore, the ideal target of angiogenesis is probably yet to be identified.
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