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Sano, Tetsuro,Lin, Huai,Chen, Xiashan,Langford, Lauren A.,Bondy, Dimpy Koul Melissa L.,Hess, Kenneth R.,Myers, Jeffery N.,Hong, Yong-Kil,Yung, W.K. Alfred,Steck, Peter A. 가톨릭대학교 2000 Bulletin of The Catholic Research Institutes of Me Vol.28 No.-
MMAC/PTEN, a tumor suppressor gene located on chromosome 10q, has recently been shown to act as a phosphatidylinositol 3,4,5-triphosphate phosphatase and to modulate cell growth and apoptosis. Somatic mutations of MMAC/PTEN have been reported in a number of human cancers, especially in glioblastoma multiforme (GBM), although the number of identified mutations (10-35%) is significantly lower than the frequency of LOH affecting the MMAC/PTEN locus in the specimens (75-95%). To further investigate the possible alterations that may affect MMAC/PTEN, we examined the expression of the gene by reverse transcription-PCR in a series of gliomas. A significant difference (P<0.001) was observed between the expression of MMAC/PTEN in GBMs versus lower grades of gliomas, thus mimicking the difference in allelic deletion associated with the locus in these tumors. Furthermore, Kaplan-Meier survival plots, adjusted for age and tumor grade, showed a significantly better prognosis for patients whose tumors expressed high level of MMAC/PTEN. Additionally, immunostaining of GBMs revealed little or no MMAC/PTEN expression in about two-thirds of the tumors, whereas the other approximately one-third of tumors had significantly higher levels of expression. However, in about two-thirds of the gigh-expressing specimens, a heterogeneous pattern of expression was observed, indicating that certain cells within the tumor failed to express MMAC/PTEN. The combination of these results suggest that, in addition to molecular alterations affecting the gene, altered expression of MMAC/PTEN may play a significant role in the progression of GBM and patient outcome. (Cancer Research 59:1820-1824, 1999)
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)