Luis R Féliz1, Apostolia M Tsimberidou. 1. Phase I Clinical Trials Program, Department of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Abstract
PURPOSE: To review the role of anti-vascular endothelial growth factor (anti-VEGF) therapies in the personalized medicine era. METHODS: We searched PubMed for prospective clinical trials published through October 2012 of anti-VEGF agents approved by the U.S. Food and Drug Administration or the European Medicines Agency. RESULTS: The use of anti-VEGF drugs as single agents or in combination with other targeted or cytotoxic agents was associated with improved response rates and progression-free survival. Anti-VEGF therapy exerts its action by blocking tumor vessel formation and, thus, proliferation. Some investigators demonstrated modest to no improvement in overall survival, although the maintenance of anti-VEGF therapy beyond progression was shown to result in longer overall survival. The use of anti-VEGF therapy was associated with adverse events (i.e., thromboembolism, hemorrhage, myocardial infarction, and hypertension) and transformation to a more invasive phenotype. CONCLUSIONS: The development of multikinase targeting agents that include anti-VEGF properties warrants further investigation. The role of anti-VEGF therapy is evolving in the era of personalized medicine, and its use needs to be reassessed in tumor types with effective FDA-approved targeted agents, especially in light of its relatively high cost.
PURPOSE: To review the role of anti-vascular endothelial growth factor (anti-VEGF) therapies in the personalized medicine era. METHODS: We searched PubMed for prospective clinical trials published through October 2012 of anti-VEGF agents approved by the U.S. Food and Drug Administration or the European Medicines Agency. RESULTS: The use of anti-VEGF drugs as single agents or in combination with other targeted or cytotoxic agents was associated with improved response rates and progression-free survival. Anti-VEGF therapy exerts its action by blocking tumor vessel formation and, thus, proliferation. Some investigators demonstrated modest to no improvement in overall survival, although the maintenance of anti-VEGF therapy beyond progression was shown to result in longer overall survival. The use of anti-VEGF therapy was associated with adverse events (i.e., thromboembolism, hemorrhage, myocardial infarction, and hypertension) and transformation to a more invasive phenotype. CONCLUSIONS: The development of multikinase targeting agents that include anti-VEGF properties warrants further investigation. The role of anti-VEGF therapy is evolving in the era of personalized medicine, and its use needs to be reassessed in tumor types with effective FDA-approved targeted agents, especially in light of its relatively high cost.