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Im, Seock-Ah,Mazano, Cankelaria Gomez,Fueyo, Juan,Liu, Ta-Jen,Ke, Li-Dao,Jeong Soo Kim,Lee, Ho-Young,Steck, Peter A.,Kyritsis, Athanassios P.,Yung, W.K. Alfred 가톨릭대학교 2000 Bulletin of The Catholic Research Institutes of Me Vol.28 No.-
Presently, there is no effective treatment for glioblastoma, the most malignant and common brain tumor. Angiogenic factors are potentially optimal targets for therapeutic strategies because they are essential for tumor growth and progression. In this study, we sought a strategy for efficiently delivering and antisinse cDNA molecule of the vascular endothelial growth factor(VEGF) to glioma cells. The recombinant adenoviral vector Ad5CMV-αVEGF carried the coding sequence of wild-type VEGF165 cDNA in an antisense orientation. Infection of U-87 MG malignant glioma cells with the Ad5CMV-αVEGF resulted in reduction of the level of the endogenous VEGF mRNA and drastically decreased the production of the targeted secretory form of the VEGF protein. Treatment of human glioma tumors established in nude mice with intralesional injection of Ad5CMV-αVEGF inhibited tumor growth. Taken together, these findings indicate that the efficient down-regulation of the VEGF produced by tumoral cells using antisense strategies has an antitumor effect in vivo, This is the first time that an adenoviral vector is used to transfer antisense VEGF sequence into glioma cells in an animal model, and our results suggest that this system may have a clinical and therapeutic utility. (Cancer Researcg 59:895-900, 1999)
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Tumor Suppressor Gene Therapy Strategies in Human Brain Tumor
Gomez-Manzano, Candeleria,Kyritsis, Athanassios,Alfred Yung, W. K.,Fueyo, Juan 가톨릭 의과학연구원 1997 가톨릭 의과학연구원 국제학술대회 Vol.1 No.-
Wild-type p53 is involved in several aspects of cell cycle control and suppression of transformation. inducing either apoptosis or G block in cell cycle progression. Using a recombinant adenovirus containting the wild-type p53 cDNA, the biological effects of the newly expressed wild-type p53 protein were examined in six human glioma cell lines. Three cell lines(U-251 MG. U0373 MG. and A-172) expressed endogenous mutant p53. and the other three(U-87 MG EFC-2, and D54 MG) expressed wild-type p53. The restoration of normal p53-encoded protein in the mutant cell lines induecd apoptosis as assessed by morphological studies using nuclear staining. electron microscopy. and flow cytometric assays. In wild-type p53 cell lines. However, the over expression of wild-type p53 did not result in apoptosis but inhibited cellular proliferation rather drastically and modified the neoplastic phenotype. This study shows that over-expression of wild-type p53 protein by an adenoviral vector induces apoptosis in mutant glioma cells as well as growth arrest in wild-type glioma cells.
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