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dc.contributor.author Faury D
dc.contributor.author Nantel A
dc.contributor.author Dunn SE
dc.contributor.author Guiot MC
dc.contributor.author Haque T
dc.contributor.author Hauser, Péter
dc.contributor.author Garami, Miklós
dc.contributor.author Bognár, László
dc.contributor.author Hanzély Z
dc.contributor.author Liberski PP
dc.contributor.author Lopez-Aguilar E
dc.contributor.author Valera ET
dc.contributor.author Tone LG
dc.contributor.author Carret AS
dc.contributor.author Del Maestro RF
dc.contributor.author Gleave M
dc.contributor.author Montes JL
dc.contributor.author Pietsch T
dc.contributor.author Albrecht S
dc.contributor.author Jabado N
dc.date.accessioned 2017-05-22T07:14:32Z
dc.date.available 2017-05-22T07:14:32Z
dc.date.issued 2007
dc.identifier 34247131323
dc.identifier.citation pagination=1196-1208; journalVolume=25; journalIssueNumber=10; journalTitle=JOURNAL OF CLINICAL ONCOLOGY;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/4131
dc.identifier.uri doi:10.1200/JCO.2006.07.8626
dc.description.abstract PURPOSE: Pediatric glioblastoma (pGBM) is a rare, but devastating brain tumor. In contrast to GBM in adults (aGBM), little is known about the mechanisms underlying its development. Our aim is to gain insight into the molecular pathways of pGBM. MATERIALS AND METHODS: Thirty-two pGBM and seven aGBM samples were investigated using biochemical and transcriptional profiling. Ras and Akt pathway activation was assessed through the phosphorylation of downstream effectors, and gene expression profiles were generated using the University Health Network Human 19K cDNA arrays. Results were validated using real-time polymerase chain reaction and immunohistochemistry and compared with existing data sets on aGBM. RESULTS: There are at least two subsets of pGBM. One subset, associated with Ras and Akt pathway activation, has very poor prognosis and exhibits increased expression of genes related to proliferation and to a neural stem-cell phenotype, similar to findings in aggressive aGBM. This subset was still molecularly distinguishable from aGBM after unsupervised and supervised analysis of expression profiles. A second subset, with better prognosis, is not associated with activation of Akt and Ras pathways, may originate from astroglial progenitors, and does not express gene signatures and markers shown to be associated with long-term survival in aGBM. Both subsets of pGBM show overexpression of Y- box-protein-1 that may help drive oncogenesis in this tumor. CONCLUSION: Our work, the first study of gene expression profiles in pGBM, provides valuable insight into active pathways and targets in a cancer with minimal survival, and suggests that these tumors cannot be understood exclusively through studies of aGBM.
dc.relation.ispartof urn:issn:0732-183X
dc.title Molecular Profiling Identifies Prognostic Subgroups of Pediatric Glioblastoma and Shows Increased YB-1 Expression in Tumors.
dc.type Journal Article
dc.date.updated 2017-03-23T11:52:05Z
dc.language.rfc3066 en
dc.identifier.mtmt 1082221
dc.identifier.wos 000245677300008
dc.identifier.pubmed 17401009
dc.contributor.department SE/AOK/K/II. Sz. Gyermekgyógyászati Klinika
dc.contributor.institution Semmelweis Egyetem


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