5 306

Cited 26 times in

Prediction for response duration to epidermal growth factor receptor-tyrosine kinase inhibitors in EGFR mutated never smoker lung adenocarcinoma

DC FieldValueLanguage
dc.contributor.author조병철-
dc.contributor.author김대준-
dc.contributor.author김세규-
dc.contributor.author김주항-
dc.contributor.author김혜련-
dc.contributor.author심효섭-
dc.contributor.author임선민-
dc.contributor.author장준-
dc.date.accessioned2015-01-06T16:34:20Z-
dc.date.available2015-01-06T16:34:20Z-
dc.date.issued2014-
dc.identifier.issn0169-5002-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/98356-
dc.description.abstractOBJECTIVES: Among non-small cell lung cancer (NSCLC) patients harboring activating epidermal growth factor receptor (EGFR) mutations, ∼ 20-30% exhibit de novo resistance to EGFR-tyrosine kinase inhibitor (TKI). The aim of this study was to examine whether mutations in the EGFR-downstream genes may be associated with de novo resistance to EGFR-TKIs in EGFR mutation-positive patients. MATERIALS AND METHODS: Sixty-eight never-smoker adenocarcinoma patients with an activating EGFR mutation were included in the mutational analysis and 55 patients treated with EGFR-TKIs were analyzed for the treatment outcomes to EGFR-TKIs. We concurrently analyzed mutations in PIK3CA, PTEN, AKT and STK11, which are all EGFR-downstream genes. Mutations in PIK3CA, PTEN, AKT, and STK11 were analyzed by polymerase chain reaction-based sequencing. RESULTS: PIK3CA mutations were detected in 4.4% (3/68) of patients, PTEN mutations in 16.1% (11/68), AKT mutations in 5.9% (4/68), and STK11 mutations in 13.2% (9/68). One patient with an activating exon 21 L858R mutation concomitantly had an exon 20 T790M mutation in EGFR. The proportion of patients who had mutations in EGFR-downstream genes was 32.4% (22/68). When we analyzed the treatment outcome of 55 patients treated with EGFR-TKI, the presence of mutations in EGFR-downstream genes correlated with a poor overall response rate to EGFR-TKIs (63.6 vs.14.5% in patients with mutation in EGFR-downstream gene, P<0.0001), shorter median progression-free survival (12.0 vs. 3.0 months, P=0.060), and shorter median overall survival (18.9 vs. 25.0 months, P=0.048). CONCLUSION: Mutations in the EGFR-downstream genes may confer resistance to EGFR-TKIs and result in poor treatment outcomes in never-smoker adenocarcinoma patients with activating EGFR mutations.-
dc.description.statementOfResponsibilityopen-
dc.format.extent374~382-
dc.relation.isPartOfLUNG CANCER-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdenocarcinoma/diagnosis*-
dc.subject.MESHAdenocarcinoma/drug therapy-
dc.subject.MESHAdenocarcinoma/mortality-
dc.subject.MESHAdult-
dc.subject.MESHAged-
dc.subject.MESHClass I Phosphatidylinositol 3-Kinases-
dc.subject.MESHDNA Mutational Analysis-
dc.subject.MESHDrug Resistance, Neoplasm/genetics-
dc.subject.MESHFemale-
dc.subject.MESHHumans-
dc.subject.MESHLung/diagnostic imaging-
dc.subject.MESHLung/drug effects*-
dc.subject.MESHLung/pathology-
dc.subject.MESHLung Neoplasms/diagnosis*-
dc.subject.MESHLung Neoplasms/drug therapy*-
dc.subject.MESHLung Neoplasms/mortality-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHMutation/genetics-
dc.subject.MESHOncogene Protein v-akt/genetics-
dc.subject.MESHPTEN Phosphohydrolase/genetics-
dc.subject.MESHPhosphatidylinositol 3-Kinases/genetics-
dc.subject.MESHPrognosis-
dc.subject.MESHProtein Kinase Inhibitors/therapeutic use*-
dc.subject.MESHProtein-Serine-Threonine Kinases/genetics-
dc.subject.MESHRadiography-
dc.subject.MESHReceptor, Epidermal Growth Factor/antagonists & inhibitors-
dc.subject.MESHReceptor, Epidermal Growth Factor/genetics-
dc.subject.MESHSmoking-
dc.subject.MESHSurvival Analysis-
dc.subject.MESHTreatment Outcome-
dc.subject.MESHTumor Burden/drug effects-
dc.titlePrediction for response duration to epidermal growth factor receptor-tyrosine kinase inhibitors in EGFR mutated never smoker lung adenocarcinoma-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Thoracic & Cardiovascular Surgery (흉부외과학)-
dc.contributor.googleauthorHye Ryun Kim-
dc.contributor.googleauthorByoung Chul Cho-
dc.contributor.googleauthorHyo Sup Shim-
dc.contributor.googleauthorSun Min Lim-
dc.contributor.googleauthorSe Kyu Kim-
dc.contributor.googleauthorJoon Chang-
dc.contributor.googleauthorDae Joon Kim-
dc.contributor.googleauthorJoo Hang Kim-
dc.identifier.doi10.1016/j.lungcan.2013.12.011-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA03822-
dc.contributor.localIdA00368-
dc.contributor.localIdA00602-
dc.contributor.localIdA00945-
dc.contributor.localIdA01166-
dc.contributor.localIdA02219-
dc.contributor.localIdA03369-
dc.contributor.localIdA03472-
dc.relation.journalcodeJ02174-
dc.identifier.eissn1872-8332-
dc.identifier.pmid24468202-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0169500213005813-
dc.subject.keywordAKT1, 2-
dc.subject.keywordEGFR-
dc.subject.keywordLung adenocarcinoma-
dc.subject.keywordPI3KCA-
dc.subject.keywordPTEN-
dc.subject.keywordResponse to EGFR TKIs-
dc.subject.keywordSTK11 mutations-
dc.contributor.alternativeNameCho, Byoung Chul-
dc.contributor.alternativeNameKim, Dae Joon-
dc.contributor.alternativeNameKim, Se Kyu-
dc.contributor.alternativeNameKim, Joo Hang-
dc.contributor.alternativeNameKim, Hye Ryun-
dc.contributor.alternativeNameShim, Hyo Sup-
dc.contributor.alternativeNameLim, Sun Min-
dc.contributor.alternativeNameChang, Joon-
dc.contributor.affiliatedAuthorCho, Byoung Chul-
dc.contributor.affiliatedAuthorKim, Dae Joon-
dc.contributor.affiliatedAuthorKim, Se Kyu-
dc.contributor.affiliatedAuthorKim, Joo Hang-
dc.contributor.affiliatedAuthorKim, Hye Ryun-
dc.contributor.affiliatedAuthorShim, Hyo Sup-
dc.contributor.affiliatedAuthorLim, Sun Min-
dc.contributor.affiliatedAuthorChang, Joon-
dc.rights.accessRightsfree-
dc.citation.volume83-
dc.citation.number3-
dc.citation.startPage374-
dc.citation.endPage382-
dc.identifier.bibliographicCitationLUNG CANCER, Vol.83(3) : 374-382, 2014-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Thoracic and Cardiovascular Surgery (흉부외과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.