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DC Field | Value | Language |
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dc.contributor.author | Luwor, Rodney B | en |
dc.contributor.author | Zhu, Hong-Jian | en |
dc.contributor.author | Walker, Francesca | en |
dc.contributor.author | Vitali, Angela A | en |
dc.contributor.author | Perera, Rushika M | en |
dc.contributor.author | Burgess, Antony W | en |
dc.contributor.author | Scott, Andrew M | en |
dc.contributor.author | Johns, Terrance G | en |
dc.date.accessioned | 2015-05-15T22:58:16Z | |
dc.date.available | 2015-05-15T22:58:16Z | |
dc.date.issued | 2004-08-12 | en |
dc.identifier.citation | Oncogene; 23(36): 6095-104 | en |
dc.identifier.govdoc | 15221011 | en |
dc.identifier.other | PUBMED | en |
dc.identifier.uri | https://ahro.austin.org.au/austinjspui/handle/1/9760 | en |
dc.description.abstract | Mutations 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.iso | en | en |
dc.subject.other | Animals | en |
dc.subject.other | Cell Cycle | en |
dc.subject.other | Cell Division | en |
dc.subject.other | Cell Line | en |
dc.subject.other | Cell Survival | en |
dc.subject.other | Dimerization | en |
dc.subject.other | Genes, erbB | en |
dc.subject.other | Interleukin-3.pharmacology | en |
dc.subject.other | Mice | en |
dc.subject.other | Neoplasms.genetics | en |
dc.subject.other | Receptor, Epidermal Growth Factor.genetics.metabolism | en |
dc.subject.other | Sequence Deletion | en |
dc.subject.other | Signal Transduction | en |
dc.title | The tumor-specific de2-7 epidermal growth factor receptor (EGFR) promotes cells survival and heterodimerizes with the wild-type EGFR. | en |
dc.type | Journal Article | en |
dc.identifier.journaltitle | Oncogene | en |
dc.identifier.affiliation | Tumour Targeting Program, Ludwig Institute for Cancer Research, Melbourne Branch, Austin Hospital, Heidelberg 3084, Australia | en |
dc.identifier.doi | 10.1038/sj.onc.1207870 | en |
dc.description.pages | 6095-104 | en |
dc.relation.url | https://pubmed.ncbi.nlm.nih.gov/15221011 | en |
dc.type.austin | Journal Article | en |
local.name.researcher | Scott, Andrew M | |
item.openairetype | Journal Article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.grantfulltext | none | - |
item.fulltext | No Fulltext | - |
item.cerifentitytype | Publications | - |
item.languageiso639-1 | en | - |
crisitem.author.dept | Molecular Imaging and Therapy | - |
crisitem.author.dept | Olivia Newton-John Cancer Research Institute | - |
Appears in Collections: | Journal articles |
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