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Glioblastoma is among the most vascular of neoplasms, its excess vasculature induced by several factors produced by tumor cells. Folkman1 envisioned antiangiogenic treatment as a means of stopping tumor growth by starving tumors of oxygen and nutrients. Accumulating evidence, however, supports the hypothesis of Jain et al.2 that antiangiogenic treatment can lead to vascular normalization, ridding tumors of bulky malformed vessels, reducing fluid transudation, decreasing intratumoral pressure, and sometimes improving oxygenation.
Bevacizumab (BEV), a monoclonal antibody against the vascular endothelial growth factor A (VEGF-A) protein, was approved in the United States for treatment of recurrent glioblastoma in May 2009. It is given IV, generally every 2–3 weeks.
Some say that the most important advances in medicine do not require a statistician. Certainly one does not need to treat more than a few patients with glioblastoma with BEV before appreciating its activity as evident on MRI. This activity establishes the importance of VEGF-A in glioblastoma angiogenesis. The objective responses seen in ∼30%–60% are those cases where the product of perpendicular diameters of the enhancing component decreases by 50%. Some benefit is evident in additional cases as lesser decreases in size, fading of enhancement, and decreases in edema and mass effect. However, responses …
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