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Pathways mediating VEGF-independent tumor angiogenesis
Authors:Napoleone Ferrara
Affiliation:1. Laboratory of Angiogenesis & Neurovascular Link, Vesalius Research Center, VIB, K.U. Leuven, Campus Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium;2. Laboratory of Angiogenesis & Neurovascular Link, Vesalius Research Center, VIB, Leuven, Belgium;1. The Clinical Laboratory of Xi’an No.1 Hospital, Xi’an 710002, Shaanxi, China;2. The Cardiac Intervention Room of Xi’an No.1 Hospital, Xi’an 710002, Shaanxi, China;3. Department of Cadre’s Ward of Xi’an No.1 Hospital, Xi’an 710002, Shaanxi, China;4. Department of Clinical Laboratory, Shaanxi Friendship Hospital, Xi’an 710068, Shaanxi, China;1. Department of Biology, Johns Hopkins University, 3400 North Charles Street, Baltimore, MD 21218, USA;1. Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, CZ-625 00 Brno, Czech Republic;2. Central European Institute of Technology, Brno University of Technology, Technicka 3058/10, CZ-616 00 Brno, Czech Republic;3. Department of Chemistry and Biochemistry, Mendel University in Brno, Zemedelska 1, CZ-613 00 Brno, Czech Republic;1. Swiss Institute for Experimental Cancer Research (ISREC), School of Life Sciences, École Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland;2. Translational Medicine Oncology, MedImmune, Gaithersburg, MD 20878, USA
Abstract:FDA approval of several inhibitors of the VEGF pathway has enabled significant advances in the therapy of cancer and neovascular age-related macular degeneration. However, similar to other therapies, inherent/acquired resistance to anti-angiogenic drugs may occur in patients, leading to disease progression. So far the lack of predictive biomarkers has precluded identification of patients most likely to respond to such treatments. Recent suggest that both tumor and non-tumor (stromal) cell types are involved in the reduced responsiveness to the treatments. The present review examines the role of tumor- as well as stromal cell-derived pathways involved in tumor growth and in refractoriness to anti-VEGF therapies.
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