Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9760
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dc.contributor.authorLuwor, Rodney Ben
dc.contributor.authorZhu, Hong-Jianen
dc.contributor.authorWalker, Francescaen
dc.contributor.authorVitali, Angela Aen
dc.contributor.authorPerera, Rushika Men
dc.contributor.authorBurgess, Antony Wen
dc.contributor.authorScott, Andrew Men
dc.contributor.authorJohns, Terrance Gen
dc.date.accessioned2015-05-15T22:58:16Z
dc.date.available2015-05-15T22:58:16Z
dc.date.issued2004-08-12en
dc.identifier.citationOncogene; 23(36): 6095-104en
dc.identifier.govdoc15221011en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9760en
dc.description.abstractMutations of the epidermal growth factor receptor (EGFR) gene are found at a relatively high frequency in glioma, with the most common being the de2-7 EGFR (or EGFRvIII). This mutation arises from an in-frame deletion of exons 2-7, which removes 267 amino acids from the extracellular domain of the receptor. Despite being unable to bind ligand, the de2-7 EGFR is constitutively active and imparts a significant in vivo growth advantage to glioma cells. In order to examine the signalling pathways activated by the de2-7 EGFR and its biological effects in an in vitro system, the de2-7 EGFR gene was transfected into the murine IL-3-dependent pro-B-cell line BaF/3. Expression of the de2-7 EGFR enhanced the survival of BaF/3 cells in the absence of IL-3 by reducing apoptosis in a phosphatidylinositol 3-kinase (PI3-K)-dependent manner. Interestingly, while de2-7 EGFR also enhanced proliferation of BaF/3 cells in low levels of IL-3, this effect was independent of PI3-K. Survival and proliferation were further enhanced when BaF/3 cells were cotransfected with the de2-7 and wt EGFR. This was due to heterodimerization between the de2-7 and wt EGFR leading to trans-phosphorylation of the wt EGFR. This observation is directly relevant to glioma where de2-7 and wt EGFR appear to be coexpressed. Thus, expression of de2-7 EGFR in BaF/3 cells provides an in vitro model for evaluating the signalling pathways activated by this receptor.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherCell Cycleen
dc.subject.otherCell Divisionen
dc.subject.otherCell Lineen
dc.subject.otherCell Survivalen
dc.subject.otherDimerizationen
dc.subject.otherGenes, erbBen
dc.subject.otherInterleukin-3.pharmacologyen
dc.subject.otherMiceen
dc.subject.otherNeoplasms.geneticsen
dc.subject.otherReceptor, Epidermal Growth Factor.genetics.metabolismen
dc.subject.otherSequence Deletionen
dc.subject.otherSignal Transductionen
dc.titleThe tumor-specific de2-7 epidermal growth factor receptor (EGFR) promotes cells survival and heterodimerizes with the wild-type EGFR.en
dc.typeJournal Articleen
dc.identifier.journaltitleOncogeneen
dc.identifier.affiliationTumour Targeting Program, Ludwig Institute for Cancer Research, Melbourne Branch, Austin Hospital, Heidelberg 3084, Australiaen
dc.identifier.doi10.1038/sj.onc.1207870en
dc.description.pages6095-104en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/15221011en
dc.type.austinJournal Articleen
local.name.researcherScott, Andrew M
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
crisitem.author.deptMolecular Imaging and Therapy-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
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