title: Inhibition of angiogenesis via FGF-2 blockage in primitive and bone metastatic renal cell carcinoma.
abstract: BACKGROUND
  Fibroblast growth factor-2 (FGF-2) has a role in the angiogenesis induced by renal carcinoma.
  
  
  METHODS
  Blockage of FGF-2 by an antisense oligonucleotide (ASO) or by a mouse neutralizing anti-human FGF-2 monoclonal antibody (anti-FGF-2-mAb) was evaluated on a cell line isolated from a renal carcinoma bone metastasis (CRBM-1990), on Caki-1 and ACHN cells. Cocultures of endothelial cells and ASO- or mAb-treated carcinoma lines were investigated.
  
  
  RESULTS
  Anti-FGF-2-mAb treatment induced a 33% reduction of FGF-2 released by ACHN, a 31% reduction of FGF-2 released by Caki-1, and a 70% reduction of FGF-2 released by CRBM-1990. ASO treatment did not inhibit endothelial cell proliferation. In contrast, anti-FGF-2-mAb significantly decreased endothelial cells proliferation induced by ACHN and CRBM-1990. The inhibition of endothelial cell growth was reverted by recombinant FGF-2.
  
  
  CONCLUSIONS
  Modulation of FGF-2 production by renal cell carcinoma with a blocking mAb produced a significant inhibition of endothelial cell growth.
authors.affiliation: Laboratory for Pathophysiology of Orthopedic Implants, Istituti Ortopedici Rizzoli, Bologna, Italy. elisabetta.cenni@ior.it
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Cenni
authors.forename: Francesca
authors.initials: F
authors.lastname: Perut
authors.forename: Donatella
authors.initials: D
authors.lastname: Granchi
authors.forename: Sofia
authors.initials: S
authors.lastname: Avnet
authors.forename: Ilaria
authors.initials: I
authors.lastname: Amato
authors.forename: Maria Luisa
authors.initials: ML
authors.lastname: Brandi
authors.forename: Armando
authors.initials: A
authors.lastname: Giunti
authors.forename: Nicola
authors.initials: N
authors.lastname: Baldini
mesh_terms: D000911:Antibodies, Monoclonal / Q000276:immunology / Q000494:pharmacology; D001859:Bone Neoplasms / Q000098:blood supply* / Q000378:metabolism / Q000556:secondary* / Q000628:therapy; D002292:Carcinoma, Renal Cell / Q000098:blood supply* / Q000378:metabolism / Q000556:secondary / Q000628:therapy; D048708:Cell Growth Processes / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D045744:Cell Line, Tumor; D042783:Endothelial Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D016222:Fibroblast Growth Factor 2 / Q000037:antagonists & inhibitors* / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D006801:Humans; D007680:Kidney Neoplasms / Q000098:blood supply* / Q000378:metabolism / Q000628:therapy; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000628:therapy; D016376:Oligonucleotides, Antisense / Q000235:genetics / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics
chemical_list: D000911:Antibodies, Monoclonal; D016376:Oligonucleotides, Antisense; D012333:RNA, Messenger; D016222:Fibroblast Growth Factor 2