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  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/123456789/23249
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dc.contributor.authorJin, X.en
dc.contributor.authorNguyen, D.en
dc.contributor.authorZhang, W. W.en
dc.contributor.authorKyritsis, A. P.en
dc.contributor.authorRoth, J. A.en
dc.date.accessioned2015-11-24T19:31:20Z-
dc.date.available2015-11-24T19:31:20Z-
dc.identifier.issn0008-5472-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/23249-
dc.rightsDefault Licence-
dc.subjectAdenoviridae/*geneticsen
dc.subjectAnimalsen
dc.subjectBase Sequenceen
dc.subjectCarcinoma, Non-Small-Cell Lung/*metabolism/therapy/virologyen
dc.subjectCarrier Proteins/genetics/*metabolism/physiologyen
dc.subjectCell Cycle/*geneticsen
dc.subjectCell Division/geneticsen
dc.subjectCyclin-Dependent Kinase Inhibitor p16en
dc.subjectCyclin-Dependent Kinases/metabolismen
dc.subjectGene Deletionen
dc.subjectGenes, Tumor Suppressor/*physiologyen
dc.subjectGenetic Vectors/*physiologyen
dc.subjectHumansen
dc.subjectLung Neoplasms/*metabolism/therapy/virologyen
dc.subjectMiceen
dc.subjectMice, Inbred BALB Cen
dc.subjectMice, Nudeen
dc.subjectMolecular Sequence Dataen
dc.subjectTransfection/methodsen
dc.subjectTumor Cells, Cultureden
dc.titleCell cycle arrest and inhibition of tumor cell proliferation by the p16INK4 gene mediated by an adenovirus vectoren
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/7614457-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate1995-
heal.abstractThe p16INK4 (MTS1) gene has many features of a tumor suppressor gene. It maps to 9p21, a region of frequent loss of heterozygosity in a variety of tumor types. It encodes an inhibitor of cyclin-dependent kinase 4, and its homozygous deletion is common in tumor-derived cell lines. To examine its tumor suppressive function and its potential in cancer gene replacement therapy, wild-type p16INK4 was expressed in an adenovirus-derived gene delivery system and introduced into lung cancer cell lines that do not express p16INK4. Expression of the introduced p16INK4 blocked tumor cell entry into S phase of the cell cycle and inhibited tumor proliferation both in vitro and in vivo. These observations strongly support that p16INK4 is a tumor suppressor gene and is a candidate for cancer gene replacement therapy.en
heal.journalNameCancer Resen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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