Experimental study of therapy effects of anti -VEGF antibody on osteosarcoma / 中华外科杂志
Chinese Journal of Surgery
;
(12): 225-227, 2002.
Article
Dans Chinois
| WPRIM
| ID: wpr-314891
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of anti-VEGF antibody on angiogenesis induced by osteosarcoma OS-732 cell line and tumor growth.</p><p><b>METHODS</b>With a tumor model on the chick embryo chorioallantoic membrane (CAM), the inhibition of angiogenesis and tumor growth by anti-VEGF antibody were observed under a stero-microscope and a light microscope. Furthermore, the proliferation and apoptosis in tumor cells and endothelial cells (EC) were studied by TdT-mediated duTP nick and labeling (TUNEL) and immunohistochemical staining using proliferating cell nuclear antigen (PCNA) monoclonal antibody.</p><p><b>RESULTS</b>VEGF polyclonal antibody administration in tumor-bearing chick embryo resulted in growth arrest of xenografts and a markedly reduction in the new capillaries which converged upon the tumor. The tumor cell apoptotic index was higher in the anti-VEGF antibody treated group than the negative control group, but the proliferation index was not significantly different between them. At the same time, increased apoptosis and decreased proliferation in EC were also noted.</p><p><b>CONCLUSION</b>VEGF polyclonal antibody is able to inhibit the angiogenesis induced by OS-732 obviously, probably by the mechanism of inhibition of EC proliferation and promotion of their apoptosis, furtherly, which may contribute to the apoptosis of tumor cells and result in suppression of tumor growth.</p>
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Thérapeutique
/
Tumeurs osseuses
/
Endothélium vasculaire
/
Ostéosarcome
/
Division cellulaire
/
Facteurs de croissance endothéliale
/
Lymphokines
/
Apoptose
/
Biologie cellulaire
/
Facteurs de croissance endothéliale vasculaire
Type d'étude:
Étude pronostique
Limites du sujet:
Animaux
langue:
Chinois
Texte intégral:
Chinese Journal of Surgery
Année:
2002
Type:
Article
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