title: Modified model of VX2 tumor overexpressing vascular endothelial growth factor.
abstract: OBJECTIVE
  To determine whether upregulated expression of vascular endothelial growth factor (VEGF) in VX2 cells can increase vessel density (VD) and reduce tumor necrosis.
  
  
  METHODS
  The VX2 cell line was transfected with expression vectors containing cDNA for rabbit VEGF. Stable clones producing rabbit VEGF (VEGF-VX2) were selected. VEGF-VX2 cells (n = 5 rabbits) or nontransfected VX2 cells (controls; n = 5 rabbits) were implanted into leg muscle of 10 rabbits. The animals were sacrificed at day 21. Tumor volume, percentage of necrosis, VD, and VEGF concentration in tumor protein extract were quantified.
  
  
  RESULTS
  Overexpression of VEGF by VX2 cells augmented tumor implantation efficiency 100% and favored cyst formation. The tumor volume was significantly larger for VEGF-VX2 transfected tumors versus controls (P = .0143). Overexpression of VEGF in VX2 cells significantly increased the VD of the tumors (P = .0138). The percentage of necrosis was reduced in VEGF-VX2 tumors versus controls (19.5% vs 38.5 %; P = .002). VEGF concentration in VEGF-VX2 tumors was significantly higher than in control tumors (P = .041) and was correlated with tumor volume (ρ = .883, P = .012).
  
  
  CONCLUSIONS
  The overexpression of VEGF increased tumor growth and vascularization, favored cyst formation, and reduced tumor necrosis. This new phenotype of the VX2 tumor may offer some advantages over classic models of VX2 tumor for evaluating anticancer therapies.
authors.affiliation: ArchimMed Paris, France.
authors.forename: Florentina
authors.initials: F
authors.lastname: Pascale
authors.forename: Saida-Homayra
authors.initials: SH
authors.lastname: Ghegediban
authors.forename: Michel
authors.initials: M
authors.lastname: Bonneau
authors.forename: Laurent
authors.initials: L
authors.lastname: Bedouet
authors.forename: Julien
authors.initials: J
authors.lastname: Namur
authors.forename: Valentin
authors.initials: V
authors.lastname: Verret
authors.forename: Isabelle
authors.initials: I
authors.lastname: Schwartz-Cornil
authors.forename: Michel
authors.initials: M
authors.lastname: Wassef
authors.forename: Alexandre
authors.initials: A
authors.lastname: Laurent
mesh_terms: D000818:Animals; D014408:Biomarkers, Tumor / Q000378:metabolism; D001808:Blood Vessels / Q000378:metabolism* / Q000473:pathology; D045744:Cell Line, Tumor; D005838:Genotype; D007150:Immunohistochemistry; D019042:Muscle Neoplasms / Q000098:blood supply / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D009336:Necrosis; D018297:Neoplasms, Cystic, Mucinous, and Serous / Q000098:blood supply / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D009389:Neovascularization, Pathologic; D010641:Phenotype; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D011817:Rabbits; D013997:Time Factors; D014162:Transfection; D047368:Tumor Burden; D015854:Up-Regulation; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D014408:Biomarkers, Tumor; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D042461:Vascular Endothelial Growth Factor A