title: Importance of fibroblast growth factor receptor in neovascularization and tumor escape from antiangiogenic therapy.
abstract: Therapeutic inhibition of pathways involved in angiogenesis has become the standard of care in renal cell carcinoma (RCC). Most currently available antiangiogenic agents inhibit the vascular endothelial growth factor (VEGF) pathway. Although these drugs have produced exciting benefits, some tumors do not respond to these agents. In addition most if not all tumors that initially respond will eventually develop resistance. Tumor escape from antiangiogenic therapy may include various signaling pathways that are involved in angiogenesis, including the fibroblast growth factor (FGF) signaling pathway. Emerging preclinical data suggest that FGF and VEGF act distinctly and synergistically to promote tumor vascularization. The current review discusses the role of FGF signaling in resistance to anti-VEGF therapies and outlines potential therapeutic implications.
authors.affiliation: Division of Hematology-Oncology, Massachusetts General Hospital, Boston, MA 02114, USA.
authors.forename: Philip J
authors.initials: PJ
authors.lastname: Saylor
authors.forename: Bernard
authors.initials: B
authors.lastname: Escudier
authors.forename: M Dror
authors.initials: MD
authors.lastname: Michaelson
mesh_terms: D020533:Angiogenesis Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D002292:Carcinoma, Renal Cell / Q000098:blood supply* / Q000188:drug therapy / Q000378:metabolism; D019008:Drug Resistance, Neoplasm; D006801:Humans; D007680:Kidney Neoplasms / Q000098:blood supply* / Q000188:drug therapy / Q000378:metabolism; D009389:Neovascularization, Pathologic; D020239:Receptor Cross-Talk; D017468:Receptors, Fibroblast Growth Factor / Q000378:metabolism / Q000502:physiology*; D015398:Signal Transduction
chemical_list: D020533:Angiogenesis Inhibitors; D017468:Receptors, Fibroblast Growth Factor