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Brandyn A. Castro and Manish K. Aghi

with antiangiogenic agents such as the humanized anti–vascular endothelial growth factor (VEGF) antibody bevacizumab (Avastin), which inhibits angiogenesis by neutralizing VEGF-A and prevents its interaction with VEGF receptors VEGFR1 and VEGFR2. 58 In this paper we review the preclinical evidence that led to the use of bevacizumab in glioblastoma, clinical trial results with bevacizumab and other antiangiogenic therapies for glioblastoma, the current scientific understanding of the tumor response to bevacizumab treatment, current clinical indications of bevacizumab

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Aaron J. Clark, Nicholas A. Butowski, Susan M. Chang, Michael D. Prados, Jennifer Clarke, Mei-Yin C. Polley, Michael E. Sughrue, Michael W. McDermott, Andrew T. Parsa, Mitchel S. Berger and Manish K. Aghi

G lioblastoma is a highly vascular tumor and is characterized by elevated expression of proangiogenic factors, most notably VEGF. 14 , 29 Increasing VEGF levels correlate with increasing astrocytic tumor grade and with poor prognosis. 8 , 22 , 31 In preclinical models, VEGF inhibition by monoclonal antibody causes decreased tumor vascularity and growth. 32 In clinical studies, the anti-VEGF monoclonal antibody bevacizumab (Avastin, Genentech) shows efficacy against glioblastoma. Bevacizumab alone is associated with 6-month progression-free survival in

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Weijun Wang, Walavan Sivakumar, Shering Torres, Niyati Jhaveri, Vijaya Pooja Vaikari, Alex Gong, Adam Howard, Encouse B. Golden, Stan G. Louie, Axel H. Schönthal, Florence M. Hofman and Thomas C. Chen

V ascular endothelial growth factor (VEGF) is a key regulator of tumor growth and angiogenesis. 8 , 10 This growth factor is responsible for endothelial cell proliferation, migration, survival, and the recruitment of endothelial cell progenitor cells from bone marrow to the tumor site. 29 Tumor cells, as well as cancer stem cells and infiltrating macrophages, secrete VEGF. 2 , 9 , 11 , 29 Bevacizumab (Avastin), a humanized monoclonal antibody to VEGF, was the first drug to be developed as an angiogenesis inhibitor and was approved by the US Food and

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Ashwatha Narayana, Patrick Kelly, John Golfinos, Erik Parker, Glyn Johnson, Edmond Knopp, David Zagzag, Ingeborg Fischer, Shahzad Raza, Praveen Medabalmi, Patricia Eagan and Michael L. Gruber

preclinical evidence suggesting that the blockade of VEGF can result in growth arrest and regression of the malignant glioma. 21 Advances in MR imaging have allowed us to measure and quantify changes in tissue perfusion and the integrity of the blood-brain barrier following VEGF blockade. 2 , 7 Bevacizumab (Avastin, Genentech), a humanized immunoglobulin G 1 monoclonal antibody that inhibits VEGF, has shown its effectiveness in metastatic colorectal, breast, and lung cancers. 5 , 6 , 23 In a recently reported Phase II trial, the combination of bevacizumab and irinotecan

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Sheikh A. Ali, Wassim M. McHayleh, Asif Ahmad, Rajesh Sehgal, Molly Braffet, Mohsin Rahman, Ghassan Bejjani and David M. Friedland

, repeated radiation therapy, conventional chemotherapy, and experimental treatments. The disappointing results of most therapeutic strategies in the setting of relapse 13 , 14 have led to efforts to find more effective and better tolerated treatment options, the most promising of which appears to be the combination of the newer agent irinotecan and the angiogenesis inhibitor bevacizumab. 7 , 11 , 15 Endothelial proliferation has been recognized as a marker of high-grade or aggressive glioma in several grading classifications, and it has been demonstrated that the degree

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Kee Kiat Yeo, Elena Puscasiu, Robert F. Keating and Brian R. Rood

of radiation therapy for preventing recurrence of these lesions is modest and that the potential neurocognitive effects of radiation to the temporal lobe are significant, 14 the recommendation was made to undertake treatment with the vascular endothelial growth factor inhibitor bevacizumab and the alkylating agent temozolomide in an attempt to shrink the tumor and delay or avoid radiation therapy. It was hoped that should radiotherapy become necessary, a more limited field could be achieved by reducing the tumor volume. Before therapy was started, MRI showed rapid

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Brian J. Williams, Deric M. Park and Jason P. Sheehan

P erilesional edema is a significant clinical problem. An agent that reliably abrogates this edema is dexamethasone, a potent glucocorticoid receptor agonist. 14 Animal and in vitro data indicate that VEGF is the primary mediator of peritumoral edema. 2 , 19 , 20 Dexamethasone is believed to act primarily through the glucocorticoid receptor to decrease the expression of VEGF and thereby edema. 12 Bevacizumab, a monoclonal antibody against VEGF, has been used in the treatment of recurrent glioblastoma. 8 , 15 , 21 , 24 Recently, bevacizumab has been

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Ashwatha Narayana, Deborah Gruber, Saroj Kunnakkat, John G. Golfinos, Erik Parker, Shahzad Raza, David Zagzag, Patricia Eagan and Michael L. Gruber

an important therapeutic target in the context of GBM growth and clinical or radiological progression. Bevacizumab (Avastin, Genentech) is a monoclonal antibody against VEGF-A. Currently, it is approved by the Food and Drug Administration for the treatment of recurrent GBM. The median OS in patients with recurrent GBM treated with bevacizumab in Phase II studies ranges between 8 and 9 months. 4 , 19 , 23 While bevacizumab was generally well tolerated in this setting, toxicities, including deep vein thrombosis, pulmonary embolism, intracranial bleeding, and

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Katrina A. Morris, Shazia K. Afridi, D. Gareth Evans, Anke E. Hensiek, Martin G. McCabe, Mark Kellett, Dorothy Halliday, Pieter M. Pretorius and Allyson Parry

developed cystic components with associated neurological deterioration. 22 Bevacizumab (a monoclonal anti–VEGFA antibody) has a beneficial effect on hearing and vestibular schwannoma growth in patients with NF2. 17 , 20 More than 100 NF2 patients in the United Kingdom have been treated with bevacizumab for rapidly growing schwannomas since August 2010 as part of the nationally commissioned NF2 specialist multidisciplinary service. Spinal ependymoma in NF2 is not an approved indication for bevacizumab treatment in the United Kingdom. The evidence for the use of

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John A. Boockvar, Apostolos J. Tsiouris, Christoph P. Hofstetter, Ilhami Kovanlikaya, Sherese Fralin, Kartik Kesavabhotla, Stephen M. Seedial, Susan C. Pannullo, Theodore H. Schwartz, Philip Stieg, Robert D. Zimmerman, Jared Knopman, Ronald J. Scheff, Paul Christos, Shankar Vallabhajosula and Howard A. Riina

G lioblastoma multiforme is the most aggressive human brain tumor. Until recently, there was no standard treatment for recurrent disease after combined chemotherapy and radiation treatment. Intravenously administered bevacizumab, a monoclonal antibody (IgG) to VEGF, has been used with safety and clinical success in recurrent GBM. 1 , 7 , 32 , 33 Despite these recent successes with bevacizumab, all patients progress and require salvage therapy. 37 Intraarterial chemotherapy is a known strategy of dose intensification that results in a more concentrated and