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Combined lapatinib and cetuximab enhance cytotoxicity against gefitinib-resistant lung cancer cells
DC Field | Value | Language |
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dc.contributor.author | Kim, Hwang-Phill | - |
dc.contributor.author | Han, Sae-Won | - |
dc.contributor.author | Kim, Sung-Hak | - |
dc.contributor.author | Im, Seock-Ah | - |
dc.contributor.author | Oh, Do-Youn | - |
dc.contributor.author | Bang, Yung-Jue | - |
dc.contributor.author | Kim, Tae-You | - |
dc.date.accessioned | 2010-07-05T03:42:29Z | - |
dc.date.available | 2010-07-05T03:42:29Z | - |
dc.date.created | 2020-12-21 | - |
dc.date.created | 2020-12-21 | - |
dc.date.created | 2020-12-21 | - |
dc.date.issued | 2008-03 | - |
dc.identifier.citation | Molecular Cancer Therapeutics, Vol.7 No.3, pp.607-615 | - |
dc.identifier.issn | 1535-7163 | - |
dc.identifier.other | 119500 | - |
dc.identifier.uri | https://hdl.handle.net/10371/68253 | - |
dc.description.abstract | Although non-small cell lung cancer (NSCLC) cells with somatic mutations in their epidermal growth factor receptors (EGFR) initially show a dramatic response to tyrosine kinase inhibitor (TKI), these cells eventually develop resistance to TKI. This resistance may be caused by a secondary T790M mutation in the EGFR tyrosine kinase, which leads to the substitution of methionine or threonine in 790. In this study, we show that a combination of lapatinib and cetuximab overcomes gefitinib resistance in NSCLC with the T790M mutation. e observed that T790M lung cancer cells were resistant to gefitinib, and Stat3 was persistently activated in the resistant cells. A reversible EGFR and HER2 TKI, lapatinib, decreased Stat3 activation by blocking heterodimerization of EGFR and HER2, which led to a modest increase in the inhibitory effect on gefitinib-resistant T790M cells. In addition to lapatinib, the anti-EGFR antibody, cetuximab, induced down-regulation of EGFR and apoptotic cell death in T790M cells. Finally, combined lapatinib and cetuximab treatment resulted in significantly enhanced cytotoxicity against gefitinib-resistant T790M cells in vitro and in vivo. Taken together, these data suggest that treatment with a combination of lapatinib and cetuximab, which induces dimeric dissociation and EGFR down-regulation, appears to be an effective strategy for treatment of patients with EGFR TKI-resistant NSCLC. | - |
dc.language | 영어 | - |
dc.language.iso | en | en |
dc.publisher | American Association for Cancer Research | - |
dc.title | Combined lapatinib and cetuximab enhance cytotoxicity against gefitinib-resistant lung cancer cells | - |
dc.type | Article | - |
dc.contributor.AlternativeAuthor | 임석아 | - |
dc.identifier.doi | 10.1158/1535-7163.MCT-07-2068 | - |
dc.citation.journaltitle | Molecular Cancer Therapeutics | - |
dc.identifier.wosid | 000254312800019 | - |
dc.identifier.scopusid | 2-s2.0-41649111490 | - |
dc.citation.endpage | 615 | - |
dc.citation.number | 3 | - |
dc.citation.startpage | 607 | - |
dc.citation.volume | 7 | - |
dc.identifier.sci | 000254312800019 | - |
dc.description.isOpenAccess | Y | - |
dc.contributor.affiliatedAuthor | Im, Seock-Ah | - |
dc.contributor.affiliatedAuthor | Oh, Do-Youn | - |
dc.contributor.affiliatedAuthor | Bang, Yung-Jue | - |
dc.contributor.affiliatedAuthor | Kim, Tae-You | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | GROWTH-FACTOR RECEPTOR | - |
dc.subject.keywordPlus | TYROSINE-KINASE-INHIBITOR | - |
dc.subject.keywordPlus | MONOCLONAL-ANTIBODY | - |
dc.subject.keywordPlus | ACQUIRED-RESISTANCE | - |
dc.subject.keywordPlus | ANTITUMOR-ACTIVITY | - |
dc.subject.keywordPlus | EGFR ANTIBODY | - |
dc.subject.keywordPlus | MUTATION | - |
dc.subject.keywordPlus | GW572016 | - |
dc.subject.keywordPlus | ADENOCARCINOMAS | - |
dc.subject.keywordPlus | TRANSFORMATION | - |
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