The siren song of bevacizumab: swan song or clarion call?

Bevacizumab burst onto the neuro-oncology scene in 2005 based upon dramatic responses in recurrent glioblastoma patients receiving this agent with the ineffective drug irinotecan. Acceptable toxicity and superior radiographic response rates compared with standard salvage therapy, confirmed in pivotal uncontrolled phase II trials,^1,2 led to accelerated FDA approval in 2009. Moreover, many patients were able to reduce their corticosteroid dose, suggesting steroid-sparing properties.³ Nonetheless, these reports, which focused on progression-free survival (PFS) and radiographic response, did not suggest seismic improvement in overall survival (OS). Thus, concerns persisted that the agent's apparent activity might principally or wholly reflect anti–vascular endothelial growth factor mediated stabilization of the blood–brain barrier, creating a "pseudoresponse."

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