A murine vascular endothelial growth factor antibody inhibits in vivo growth of human Caki-I renal adenocarcinoma

被引:0
作者
Dagnaes-Hansen, F
Rasmussen, LM
Tilton, R
Denner, L
Flyvbjerg, A
机构
[1] Aarhus Univ, Dept Med Microbiol & Immunol, DK-8000 Aarhus C, Denmark
[2] Aarhus Kommune Hosp, Dept Mol Pathol, DK-8000 Aarhus C, Denmark
[3] Aarhus Kommune Hosp, Med Res Labs M, DK-8000 Aarhus C, Denmark
[4] Texas Biotechnol Corp, Fannin, TX USA
关键词
experimental kidney neoplasms; renal cell carcinoma; vascular endothelial growth factor; VEGF; mRNA; VE-Cadherin;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
A number of studies have provided indirect evidence that angiogenesis is involved in tumour growth and metastasis formation of renal cell carcinoma (RCC). Nude mice bearing xenografts of human Caki-I RCC were treated i.p. for 3 weeks with a murine monoclonal antibody against vascular endothelial growth factor, VEGF (VEGF-ab). Tumour growth and mRNA expression of human and murine VEGF and murine VE-Cadherin in the tumours were measured. After 3 weeks of therapy, the tumour volume in the control nude mice was 548 98 mm(3) compared to the tumours in the nude mice treated with VEGF-ab (122 +/- 24 min 3. p < 0.01). Treatment with VEGF-ab significantly reduced mRNA expression of murine VEGF-120 and murine VE-Cadherin (p < 0.05 and p < 0.01, respectively). The mRNA expression of human VEGF (hVEGF165, hVEGF189) and murine VEGF (mVEGF(164)) was unchanged due to antibody treatment. The mean percentage of apoptotic cells in tumours harvested from antibody-treated animals was significantly 1, lower than in tumours from the control-treated animals (p < 0.02). These findings demonstrate for the first time that VEGF-ab significantly inhibit the growth of Caki-I RCC in vivo.
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页码:1625 / 1630
页数:6
相关论文
共 49 条
[1]  
Borgström P, 1998, PROSTATE, V35, P1
[2]   Suppression of glioblastoma angiogenicity and tumorigenicity by inhibition of endogenous expression of vascular endothelial growth factor [J].
Cheng, SY ;
Huang, HJS ;
Nagane, M ;
Ji, XD ;
Wang, DG ;
Shih, CCY ;
Arap, W ;
Huang, CM ;
Cavenee, WK .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (16) :8502-8507
[3]  
Deroanne CF, 1997, CANCER RES, V57, P5590
[4]   Elevated levels of the angiogenic cytokines basic fibroblast growth factor and vascular endothelial growth factor in sera of cancer patients [J].
Dirix, LY ;
Vermeulen, PB ;
Pawinski, A ;
Prove, A ;
Benoy, I ;
DePooter, C ;
Martin, M ;
VanOosterom, AT .
BRITISH JOURNAL OF CANCER, 1997, 76 (02) :238-243
[5]  
Drevs J, 2000, CANCER RES, V60, P4819
[6]  
Edgren M, 1999, ANTICANCER RES, V19, P869
[7]   Comparison of VEGF, VEGF-B, VEGF-C and Ang-1 mRNA regulation by serum, growth factors, oncoproteins and hypoxia [J].
Enholm, B ;
Paavonen, K ;
Ristimaki, A ;
Kumar, V ;
Gunji, Y ;
Klefstrom, J ;
Kivinen, L ;
Laiho, M ;
Olofsson, B ;
Joukov, V ;
Eriksson, U ;
Alitalo, K .
ONCOGENE, 1997, 14 (20) :2475-2483
[8]   Molecular and biological properties of vascular endothelial growth factor [J].
Ferrara, N .
JOURNAL OF MOLECULAR MEDICINE-JMM, 1999, 77 (07) :527-543
[9]   ABSENCE OF HELA-CELL CONTAMINATION IN 169 CELL LINES DERIVED FROM HUMAN TUMORS [J].
FOGH, J ;
WRIGHT, WC ;
LOVELESS, JD .
JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1977, 58 (02) :209-214
[10]  
FOLKMAN J, 1971, NEW ENGL J MED, V285, P1182