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Epidermal growth factor receptor (EGFR) exon 20 mutations in non-small-cell lung cancer and resistance to EGFR-tyrosine kinase inhibitors

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dc.contributor.authorWoo, Hyun Sun-
dc.contributor.authorAhn, Hee Kyung-
dc.contributor.authorLee, Ha Yeon-
dc.contributor.authorPark, Inkeun-
dc.contributor.authorKim, Young Saing-
dc.contributor.authorHong, Junshik-
dc.contributor.authorSym, Sun Jin-
dc.contributor.authorPark, Jinny-
dc.contributor.authorLee, Jae Hoon-
dc.contributor.authorShin, Dong Bok-
dc.contributor.authorCho, Eun Kyung-
dc.date.available2020-02-28T15:43:48Z-
dc.date.created2020-02-06-
dc.date.issued2014-12-
dc.identifier.issn0167-6997-
dc.identifier.urihttps://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/12069-
dc.description.abstractIntroduction In patients with non-small cell lung cancer (NSCLC), the predictive value of rare epidermal growth factor receptor (EGFR) exon 20 mutations in determining a patient's response to EGFR tyrosine kinase inhibitor (TKI) treatment is unclear. Patients and Methods We reviewed data for NSCLC patients harboring EGFR exon 20 mutations from two hospitals in Korea. EGFR mutations were analyzed using directional sequencing. Results We identified eight patients carrying EGFR exon 20 mutations, seven of whom had insertional mutations. Three patients carried previously unreported insertional mutations. Among six patients who were treated with EGFR TKI, one showed stable disease and three showed primary resistance. Response evaluations were not performed for the other two patients because of their clinical deterioration. Conclusions EGFR exon 20 insertional mutations, including three that were previously unreported, were associated with the poor response of patients to TKI treatment.-
dc.language영어-
dc.language.isoen-
dc.publisherSPRINGER-
dc.relation.isPartOfINVESTIGATIONAL NEW DRUGS-
dc.subjectGEFITINIB-
dc.subjectCHEMOTHERAPY-
dc.subjectMULTICENTER-
dc.subjectERLOTINIB-
dc.titleEpidermal growth factor receptor (EGFR) exon 20 mutations in non-small-cell lung cancer and resistance to EGFR-tyrosine kinase inhibitors-
dc.typeArticle-
dc.type.rimsART-
dc.description.journalClass1-
dc.identifier.wosid000345142300028-
dc.identifier.doi10.1007/s10637-014-0146-x-
dc.identifier.bibliographicCitationINVESTIGATIONAL NEW DRUGS, v.32, no.6, pp.1311 - 1315-
dc.identifier.scopusid2-s2.0-84927557113-
dc.citation.endPage1315-
dc.citation.startPage1311-
dc.citation.titleINVESTIGATIONAL NEW DRUGS-
dc.citation.volume32-
dc.citation.number6-
dc.contributor.affiliatedAuthorWoo, Hyun Sun-
dc.contributor.affiliatedAuthorAhn, Hee Kyung-
dc.contributor.affiliatedAuthorPark, Inkeun-
dc.contributor.affiliatedAuthorKim, Young Saing-
dc.contributor.affiliatedAuthorHong, Junshik-
dc.contributor.affiliatedAuthorSym, Sun Jin-
dc.contributor.affiliatedAuthorPark, Jinny-
dc.contributor.affiliatedAuthorLee, Jae Hoon-
dc.contributor.affiliatedAuthorShin, Dong Bok-
dc.contributor.affiliatedAuthorCho, Eun Kyung-
dc.type.docTypeArticle-
dc.subject.keywordAuthorEGFR-
dc.subject.keywordAuthorEGFR TKI-
dc.subject.keywordAuthorExon 20-
dc.subject.keywordAuthorNon-small cell lung carcinoma-
dc.subject.keywordPlusGEFITINIB-
dc.subject.keywordPlusCHEMOTHERAPY-
dc.subject.keywordPlusMULTICENTER-
dc.subject.keywordPlusERLOTINIB-
dc.relation.journalResearchAreaOncology-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryOncology-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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