Increased expression of the MYCN oncogene in human neuroblastoma cells and possible, new therapeutic approaches

dc.contributor.authorSchweigerer, L.en
dc.contributor.authorFotsis, T.en
dc.date.accessioned2015-11-24T19:10:50Z
dc.date.available2015-11-24T19:10:50Z
dc.identifier.issn0300-8630-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/20874
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subjectCell Division/physiologyen
dc.subjectCell Lineen
dc.subjectCell Transformation, Neoplastic/geneticsen
dc.subjectChilden
dc.subjectGene Expression Regulation, Neoplastic/physiologyen
dc.subjectGenes, myc/geneticsen
dc.subjectHumansen
dc.subjectMiceen
dc.subjectMice, Nudeen
dc.subjectNeoplasm Transplantationen
dc.subjectProto-Oncogene Proteins c-myc/geneticsen
dc.subjectTransfection/geneticsen
dc.subjectTumor Necrosis Factor-alpha/physiologyen
dc.titleIncreased expression of the MYCN oncogene in human neuroblastoma cells and possible, new therapeutic approachesen
heal.abstractHuman neuroblastomas of advanced stages often display amplification with a consecutive enhanced expression of the MYCN oncogene. Enhanced MYCN expression is thought to contribute in a causative manner to the progression of neuroblastomas, but the mechanisms by which this may occur have remained unclear. By transfecting human neuroblastoma cells that display a normal MYCN expression with the human MYCN oncogene, we have generated a cell line with enhanced MYCN expression and thereby were able to compare the biological and biochemical properties of the transfected and non-transfected cells. We have demonstrated autocrine growth factors in the MYCN-transfected, but not the non-transfected, neuroblastoma cells. Identification of the primary structures of these factors may help to develop specific antagonists in order to improve the therapy of advanced neuroblastomas. Currently, this could be done by application of genistein or tumor necrosis factor. As we could demonstrate for the first time, the dietary constituent genistein is able to inhibit the proliferation of neuroblastoma cells with enhanced and normal MYCN expression, but also that of cells derived from other solid pediatric tumors. In contrast, tumor necrosis factor is able to inhibit selectively the proliferation of neuroblastoma cells with enhanced MYCN expression. We suggest that tumor necrosis factor might improve the therapy of advanced human neuroblastomas.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.primary10.1055/s-2007-1025447-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/1942938-
heal.identifier.secondaryhttps://www.thieme-connect.de/DOI/DOI?10.1055/s-2007-1025447-
heal.journalNameKlin Padiatren
heal.journalTypepeer-reviewed-
heal.languagede-
heal.publicationDate1991-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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