. Some of these genes are involved in angiogenesis and enhance new vasculature (e.g., vascular endothelial growth factor [VEGF]), some are growth factors and stimulate cell growth (e.g., platelet-derived growth factor [PDGF] or tumor growth factor α), and
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Gary R. Hudes, Michael A. Carducci, Toni K. Choueiri, Peg Esper, Eric Jonasch, Rashmi Kumar, Kim A. Margolin, M. Dror Michaelson, Robert J. Motzer, Roberto Pili, Susan Roethke, and Sandy Srinivas
David A. Reardon, Scott Turner, Katherine B. Peters, Annick Desjardins, Sridharan Gururangan, John H. Sampson, Roger E. McLendon, James E. Herndon II, Lee W. Jones, John P. Kirkpatrick, Allan H. Friedman, James J. Vredenburgh, Darell D. Bigner, and Henry S. Friedman
radiographic responses and improved progression-free survival with bevacizumab, a humanized monoclonal antibody targeting vascular endothelial growth factor (VEGF), 7 among patients with recurrent malignant glioma. 8 – 11 However, initial enthusiasm has been
Lyndsay J. Willmott, Daniele A. Sumner, and Bradley J. Monk
endothelial growth factor (VEGF). 6 , 7 The VEGF family includes 6 closely related proteins, but the most important member in angiogenesis is VEGF-A. The mechanism through which VEGF exerts its influence seems to be multifactorial. The initial hypothesis
Andre P. Fay, Guillermo de Velasco, Thai H. Ho, Eliezer M. Van Allen, Bradley Murray, Laurence Albiges, Sabina Signoretti, A. Ari Hakimi, Melissa L. Stanton, Joaquim Bellmunt, David F. McDermott, Michael B. Atkins, Levi A. Garraway, David J. Kwiatkowski, and Toni K. Choueiri
with clinical response to treatment with vascular endothelial growth factor (VEGF)–targeted therapies (VEGF-TT), such as sunitinib or pazopanib. To examine a possible association between genomic alterations and response to VEGF-TT in RCC, we gathered
Kristen Keon Ciombor and Tanios Bekaii-Saab
treatment options for mCRC Appraise the recent clinical trial results of anti-EGFR and anti-VEGF therapies for determining optimal drug combinations and treatment sequences for mCRC Describe the 2 proven examples of genetic alterations leading to
Irbaz Bin Riaz, Saad Ullah Malik, Muhammad Husnain, Qurat Ul Ain Riaz Sipra, Warda Faridi, Farva R. Gondal, Thanh Ho, Siddhartha Yadav, Zhen Wang, and Manish Kohli
Background: Four large RCTs (ASSURE, S-TARC, PROTECT, ATLAS) tested adjuvant VEGF-TKI therapy in high risk RCC. The results were variable for efficacy and there were concerns for increased toxicity and decline in quality of life (QoL). We performed
Jasmin Eugene, Carli Nesheiwat, and Scott Overmier
Background: Vascular endothelial growth factor (VEGF) inhibitors disrupt angiogenesis and slow tumor growth but have a clinically significant side effect of hypertension. Between 9-59% of patients may develop hypertension induced VEGF inhibitors
A. Scott Paulson and Emily K. Bergsland
also has proven antitumor activity in tumors arising in the small bowel. 10 Beyond octreotide, no standard therapy exists. Additional systemic treatment options are desperately needed. Recent data suggest that vascular endothelial growth factor (VEGF
Margaret von Mehren
Medical management of soft tissue sarcomas (STS) has been restricted by the limited availability of active drugs. A plethora of new oncologic agents are now available, many of which have specific therapeutic targets. Gemcitabine and docetaxel is a combination of drugs that have limited single-agent activity. Yondelis, a novel chemotherapeutic that binds DNA and functions partially by inhibiting transcription, is being tested alone and in combination with doxorubicin. Inhibitors of mTOR, a serine/threonine kinase that regulates cell cycle activation and cell growth, are also being tested. Growth factor receptor inhibitors are being evaluated in a variety of sarcomas that have been found to express the targets. In addition, a variety of agents are being assessed in gastrointestinal stromal tumors (GIST). Single agents and agents combined with imatinib are being tested in imatinib-refractory and in metastatic GIST. The increased use of targeted agents underscores the need for understanding sarcoma biology.
Eric Jonasch and Robert J. Motzer
mutations of VHL are key drivers of clear cell RCC biology, an entirely new class of agents was developed to block the downstream consequences of hypoxia inducible factor upregulation and resultant vascular endothelial growth factor (VEGF) overproduction
