摘要：Glioblastoma multiforme (GBM) is the most common primary malignancy in adults. Despite improvements in chemoradiotherapeutic strategies, patients typically survive for less than one year [1]. Bevacizumab (BVZ), a humanized monoclonal antibody against vascular epithelial growth factor (vegf), alters the kinetics of ligand binding and has been shown to abrogate angiogenesis in different types of solid tumors [2]. The initial studies of BVZ treatment showed promising results, demonstrating decreased intratumoral enhancement and peri-tumoral edema, as well as alleviation of tumor-related symptoms. However, subsequent studies analyzing long-term outcomes were less positive, including a recent high-impact randomized, double-blinded, placebo-controlled phase 3 clinical trial which demonstrated that BVZ treatment, albeit successfully reducing disease progression, did not improve overall survival in patients with newly diagnosed GBM [3]. As such, the effects of BVZ may be transient such that tumors shortly thereafter become refractory to therapy, highlighted by increased severity of aggressive and infiltrative phenotypes. The observed efficacious yet ephemeral therapeutic benefits of BVZ indicate that targeting of vegf alone may not handcuff an entire oncogenic pathway, eventually resulting in tumor recurrence.
