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  4. Τμήμα Ιατρικής
  5. Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ
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Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/17987
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dc.contributor.authorAdachi, Y.en
dc.contributor.authorChandrasekar, N.en
dc.contributor.authorKin, Y.en
dc.contributor.authorLakka, S. S.en
dc.contributor.authorMohanam, S.en
dc.contributor.authorYanamandra, N.en
dc.contributor.authorMohan, P. M.en
dc.contributor.authorFuller, G. N.en
dc.contributor.authorFang, B.en
dc.contributor.authorFueyo, J.en
dc.contributor.authorDinh, D. H.en
dc.contributor.authorOlivero, W. C.en
dc.contributor.authorTamiya, T.en
dc.contributor.authorOhmoto, T.en
dc.contributor.authorKyritsis, A. P.en
dc.contributor.authorRao, J. S.en
dc.date.accessioned2015-11-24T18:49:37Z-
dc.date.available2015-11-24T18:49:37Z-
dc.identifier.issn0950-9232-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/17987-
dc.rightsDefault Licence-
dc.subjectAdenoviridae/geneticsen
dc.subjectApoptosisen
dc.subjectBrain Neoplasms/*pathology/therapyen
dc.subject*Cell Cycle Proteinsen
dc.subjectCyclin-Dependent Kinase Inhibitor p16/*physiologyen
dc.subject*DNA-Binding Proteinsen
dc.subjectE2F Transcription Factorsen
dc.subjectGene Expression Regulation, Neoplasticen
dc.subject*Gene Therapyen
dc.subjectGenesen
dc.subject*Genes, p16en
dc.subjectGenetic Vectors/geneticsen
dc.subjectGlioblastoma/*pathology/therapyen
dc.subjectHumansen
dc.subject*Neoplasm Invasivenessen
dc.subjectNeoplasm Proteins/*antagonists & inhibitors/genetics/physiologyen
dc.subjectNeoplasm Transplantationen
dc.subjectOligodeoxyribonucleotides, Antisense/genetics/*therapeutic useen
dc.subjectReceptors, Cell Surface/*antagonists & inhibitors/genetics/physiologyen
dc.subjectReceptors, Urokinase Plasminogen Activatoren
dc.subjectRecombinant Fusion Proteins/physiologyen
dc.subjectRetinoblastoma Protein/metabolismen
dc.subjectTranscription Factors/metabolismen
dc.subjectXenograft Model Antitumor Assaysen
dc.titleSuppression of glioma invasion and growth by adenovirus-mediated delivery of a bicistronic construct containing antisense uPAR and sense p16 gene sequencesen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1038/sj.onc.1204999-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/11791179-
heal.identifier.secondaryhttp://www.nature.com/onc/journal/v21/n1/pdf/1204999a.pdf-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2002-
heal.abstractOur previous studies showed that the urokinase-type plasminogen activator receptor (uPAR) and the p16 tumor suppressor gene play a significant role in glioma invasion. We expected that downregulation of uPAR and overexpression of p16 using a bicistronic vector might cause a additive and cooperative effect in the suppression of glioma invasion and growth. The bicistronic construct (Ad-uPAR/p16)-infected glioblastoma cell lines had significantly lower levels of uPAR and higher levels of p16 than controls. Cell cycle analysis showed the bicistronic vector caused G0/G1 arrest of the cell cycle. In vitro glioblastoma cell growth and invasiveness were inhibited in Ad-uPAR/p16-infected cells compared with controls. Ad-uPAR/p16 suppressed the tumor growth of glioblastoma cell lines in an ex vivo intracerebral tumor model and an in vivo subcutaneous tumor model. Our results support the therapeutic potential of simultaneously targeting uPAR and p16 in the treatment of gliomas.en
heal.journalNameOncogeneen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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