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Mucoepidermoid carcinoma of lung: Potential target of EGFR-directed treatment

DC Field Value Language
dc.contributor.authorHan, Sae-Won-
dc.contributor.authorKim, Hwang-Phill-
dc.contributor.authorJeon, Yoon Kyung-
dc.contributor.authorOh, Do-Youn-
dc.contributor.authorLee, Se-Hoon-
dc.contributor.authorKim, Dong-Wan-
dc.contributor.authorIm, Seock-Ah-
dc.contributor.authorChung, Doo Hyun-
dc.contributor.authorHeo, Dae Seog-
dc.contributor.authorBang, Yung-Jue-
dc.contributor.authorKim, Tae-You-
dc.date.accessioned2009-05-22T06:41:12Z-
dc.date.available2009-05-22T06:41:12Z-
dc.date.created2020-02-19-
dc.date.created2020-02-19-
dc.date.created2020-02-19-
dc.date.created2020-02-19-
dc.date.issued2008-07-
dc.identifier.citationLung Cancer, Vol.61 No.1, pp.30-34-
dc.identifier.issn0169-5002-
dc.identifier.other91893-
dc.identifier.urihttps://hdl.handle.net/10371/3705-
dc.description.abstractMucoepidermoid carcinoma (MEC) of lung is a rare malignancy of lung which originates from minor salivary glands of tracheobronchial tree. EGFR targeted therapy by inhibition of EGFR activation with the specific tyrosine kinase inhibitors (TKIs) has shown meaningful antitumor activity in patients with EGFR TK mutation and/or amplification, or in patients with adenocarcinoma. In the present study, we find that MEC has EGFR mutation in 40% (2 out of 5) of cases, and all mutations are L858R mutation. In addition, we also observed that a MEC patient well-responded to EGFR TKI in the absence of EGFR mutation or amplification. These data indicate for the first time that MEC of lung is another potential target of EGFR inhibitor, and more extended clinical investigation is warranted. (c) 2008 Elsevier Ireland Ltd. All rights reserved.-
dc.language영어-
dc.language.isoenen
dc.publisherElsevier BV-
dc.titleMucoepidermoid carcinoma of lung: Potential target of EGFR-directed treatment-
dc.typeArticle-
dc.contributor.AlternativeAuthor임석아-
dc.identifier.doi10.1016/j.lungcan.2007.11.014-
dc.citation.journaltitleLung Cancer-
dc.identifier.wosid000257934400004-
dc.identifier.scopusid2-s2.0-45649085199-
dc.citation.endpage34-
dc.citation.number1-
dc.citation.startpage30-
dc.citation.volume61-
dc.identifier.sci000257934400004-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorJeon, Yoon Kyung-
dc.contributor.affiliatedAuthorOh, Do-Youn-
dc.contributor.affiliatedAuthorKim, Dong-Wan-
dc.contributor.affiliatedAuthorIm, Seock-Ah-
dc.contributor.affiliatedAuthorChung, Doo Hyun-
dc.contributor.affiliatedAuthorHeo, Dae Seog-
dc.contributor.affiliatedAuthorBang, Yung-Jue-
dc.contributor.affiliatedAuthorKim, Tae-You-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusGROWTH-FACTOR RECEPTOR-
dc.subject.keywordPlusADENOSQUAMOUS CARCINOMA-
dc.subject.keywordPlusMUTATIONS-
dc.subject.keywordPlusCANCER-
dc.subject.keywordPlusGEFITINIB-
dc.subject.keywordPlusTUMORS-
dc.subject.keywordPlusGENE-
dc.subject.keywordPlusRAS-
dc.subject.keywordAuthormucoepidermoid carcinoma-
dc.subject.keywordAuthorEGFR-
dc.subject.keywordAuthormutation-
dc.subject.keywordAuthorgefitinib-
dc.subject.keywordAuthorlung cancer-
dc.subject.keywordAuthorL858R-
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  • Department of Medicine
Research Area Clinical Medicine

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