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Evaluation of antitumor activity of gefitinib in pediatric glioblastoma and neuroblastoma cells

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dc.contributor.author Hatziagapiou, K en
dc.contributor.author Braoudaki, M en
dc.contributor.author Karpusas, M en
dc.contributor.author Tzortzatou-Stathopoulou, F en
dc.date.accessioned 2014-06-06T06:51:18Z
dc.date.available 2014-06-06T06:51:18Z
dc.date.issued 2011 en
dc.identifier.issn 14336510 en
dc.identifier.uri http://62.217.125.90/xmlui/handle/123456789/5445
dc.relation.uri http://www.scopus.com/inward/record.url?eid=2-s2.0-80054793072&partnerID=40&md5=31abcb4b0eacd92fffb37847497635ef en
dc.subject.other epidermal growth factor receptor en
dc.subject.other epidermal growth factor receptor 2 en
dc.subject.other formazan en
dc.subject.other gefitinib en
dc.subject.other vasculotropin receptor 1 en
dc.subject.other adult en
dc.subject.other antineoplastic activity en
dc.subject.other article en
dc.subject.other cancer cell en
dc.subject.other cancer inhibition en
dc.subject.other cell viability en
dc.subject.other concentration response en
dc.subject.other drug cytotoxicity en
dc.subject.other drug screening en
dc.subject.other enzyme linked immunosorbent assay en
dc.subject.other glioblastoma en
dc.subject.other human en
dc.subject.other human cell en
dc.subject.other neuroblastoma en
dc.subject.other protein phosphorylation en
dc.subject.other Antineoplastic Agents en
dc.subject.other Cell Line, Tumor en
dc.subject.other Cell Proliferation en
dc.subject.other Cell Survival en
dc.subject.other Dose-Response Relationship, Drug en
dc.subject.other Drug Screening Assays, Antitumor en
dc.subject.other Glioblastoma en
dc.subject.other Humans en
dc.subject.other Neuroblastoma en
dc.subject.other Phosphorylation en
dc.subject.other Quinazolines en
dc.subject.other Receptor, erbB-2 en
dc.title Evaluation of antitumor activity of gefitinib in pediatric glioblastoma and neuroblastoma cells en
heal.type journalArticle en
heal.publicationDate 2011 en
heal.abstract Background: This work was undertaken to investigate the efficacy of gefitinib, an EGFR tyrosine kinase inhibitor, in tumor cell lines of the CNS by studying cell proliferation and phosphorylation of the tyrosine kinase domain of EGFR. Methods: The study included neuroblastoma (SHSY5Y) and glioblastoma (A172) cell lines. The MTT cell proliferation assay was performed in order to quantify the cytotoxic effect of gefitinib in A172 and SH-SY5Y cells, whilst ELISA assay was used to assess the effect on the phosphorylation of tyrosine residue 1068 of EGFR. Results: As the concentration of gefitinib increased, MTT conversion into formazan was observed to progressively decrease, confirming the cytotoxic activity of gefitinib. In the ELISA assay for both cell lines investigated, as the dose of gefitinib increased, a gradual decrease in EGFR tyrosine phosphorylation was detected. Conclusions: The findings of the current study could form the basis of research regarding the use of novel inhibitors in the treatment of solid tumors in pediatric patients and a shift to targeted therapy with higher efficacy and fewer side effects. en
heal.journalName Clinical Laboratory en
dc.identifier.issue 9-10 en
dc.identifier.volume 57 en
dc.identifier.spage 781 en
dc.identifier.epage 784 en


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