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Impact of cigarette smoking on response to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors in lung adenocarcinoma with activating EGFR mutations

DC FieldValueLanguage
dc.contributor.author김혜련-
dc.contributor.author배미경-
dc.contributor.author이재석-
dc.contributor.author이창영-
dc.contributor.author조병철-
dc.contributor.author강대용-
dc.contributor.author김민환-
dc.contributor.author김은영-
dc.contributor.author김주항-
dc.date.accessioned2015-01-06T16:57:29Z-
dc.date.available2015-01-06T16:57:29Z-
dc.date.issued2014-
dc.identifier.issn0169-5002-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/99097-
dc.description.abstractOBJECTIVES: The aim of this study is to evaluate the predictive impact of cigarette smoking on treatment outcomes of EGFR-tyrosine kinase inhibitors (TKIs) in lung adenocarcinoma patients with activating EGFR mutations. METHODS: We retrospectively analyzed 222 consecutive recurrent or unresectable lung adenocarcinoma patients who harbored activating EGFR mutations (exon 19 deletion or exon 21 L858R) and had received gefitinib or erlotinib. Detailed smoking histories were obtained from all patients according to a standard protocol. RESULTS: Of 222 EGFR-mutated patients, 65.3% were never-smokers, 19.8% were smokers with < 30 pack-years, and 14.9% were smokers with ≥ 30 pack-years smoking dosage. The disease control rate (DCR) and objective response rate (ORR) of smokers with ≥ 30 pack-years were significantly lower than never-smokers and smokers with < 30 pack-years (DCR, 78.8% vs. 93.1%, p = 0.016; ORR, 45.5% vs. 62.4%, p = 0.020). Smokers with ≥ 30 pack-years showed significantly shorter PFS than never-smokers (6.4 vs. 11.8 months, p = 0.001) and smokers with < 30 pack-years (6.4 vs. 11.4 months, p = 0.033), as well as shorter overall survival from the time of metastatic diagnosis than never-smokers (33.6 vs. 46.2 months, p = 0.003). There was no survival difference between smokers with < 30 pack-year and never smokers. In the multivariate analysis adjusted for age, sex, performance status, initial stage, and line of EGFR-TKI, the presence of smoking dosage ≥ 30 pack-years was an independent predictive factor for the disease progression to EGFR-TKIs (hazard ratio, 1.87; 95% confidence interval, 1.15-3.05; p = 0.012). CONCLUSIONS: Cigarette smoking dosage of ≥ 30 pack-years is an independent negative predictive factor of EGFR-TKI treatment outcome in lung adenocarcinoma patients with activating EGFR mutations.-
dc.description.statementOfResponsibilityopen-
dc.format.extent196~202-
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/drug therapy*-
dc.subject.MESHAdenocarcinoma/etiology-
dc.subject.MESHAdenocarcinoma/genetics-
dc.subject.MESHAdenocarcinoma/mortality-
dc.subject.MESHAntineoplastic Agents/pharmacology*-
dc.subject.MESHAntineoplastic Agents/therapeutic use-
dc.subject.MESHDisease-Free Survival-
dc.subject.MESHDrug Resistance, Neoplasm-
dc.subject.MESHErlotinib Hydrochloride-
dc.subject.MESHFemale-
dc.subject.MESHHumans-
dc.subject.MESHKaplan-Meier Estimate-
dc.subject.MESHLung Neoplasms/drug therapy*-
dc.subject.MESHLung Neoplasms/etiology-
dc.subject.MESHLung Neoplasms/genetics-
dc.subject.MESHLung Neoplasms/mortality-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHMultivariate Analysis-
dc.subject.MESHMutation, Missense-
dc.subject.MESHPrognosis-
dc.subject.MESHProportional Hazards Models-
dc.subject.MESHProtein Kinase Inhibitors/pharmacology*-
dc.subject.MESHProtein Kinase Inhibitors/therapeutic use-
dc.subject.MESHQuinazolines/pharmacology-
dc.subject.MESHQuinazolines/therapeutic use-
dc.subject.MESHReceptor, Epidermal Growth Factor/antagonists & inhibitors-
dc.subject.MESHReceptor, Epidermal Growth Factor/genetics*-
dc.subject.MESHRetrospective Studies-
dc.subject.MESHSequence Deletion-
dc.subject.MESHSmoking/adverse effects*-
dc.subject.MESHTreatment Outcome-
dc.titleImpact of cigarette smoking on response to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors in lung adenocarcinoma with activating EGFR mutations-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pathology (병리학)-
dc.contributor.googleauthorMin Hwan Kim-
dc.contributor.googleauthorHye Ryun Kim-
dc.contributor.googleauthorByoung Chul Cho-
dc.contributor.googleauthorMi Kyung Bae-
dc.contributor.googleauthorEun Young Kim-
dc.contributor.googleauthorChang Young Lee-
dc.contributor.googleauthorJae Seok Lee-
dc.contributor.googleauthorDae Ryong Kang-
dc.contributor.googleauthorJoo Hang Kim-
dc.identifier.doi10.1016/j.lungcan.2014.01.022-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01166-
dc.contributor.localIdA01792-
dc.contributor.localIdA03245-
dc.contributor.localIdA03822-
dc.contributor.localIdA00482-
dc.contributor.localIdA00945-
dc.contributor.localIdA00811-
dc.contributor.localIdA03072-
dc.contributor.localIdA00009-
dc.relation.journalcodeJ02174-
dc.identifier.eissn1872-8332-
dc.identifier.pmid24629638-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0169500214000580-
dc.subject.keywordCigarette smoking-
dc.subject.keywordEGFR mutation-
dc.subject.keywordEGFR-tyrosine kinase inhibitors-
dc.subject.keywordLung adenocarcinoma-
dc.subject.keywordPrognosis-
dc.subject.keywordResponse rate-
dc.contributor.alternativeNameKim, Hye Ryun-
dc.contributor.alternativeNameBae, Mi Kyung-
dc.contributor.alternativeNameLee, Jae Seok-
dc.contributor.alternativeNameLee, Chang Young-
dc.contributor.alternativeNameCho, Byoung Chul-
dc.contributor.alternativeNameKang, Dae Ryong-
dc.contributor.alternativeNameKim, Min Hwan-
dc.contributor.alternativeNameKim, Eun Young-
dc.contributor.alternativeNameKim, Joo Hang-
dc.contributor.affiliatedAuthorKim, Hye Ryun-
dc.contributor.affiliatedAuthorBae, Mi Kyung-
dc.contributor.affiliatedAuthorLee, Chang Young-
dc.contributor.affiliatedAuthorCho, Byoung Chul-
dc.contributor.affiliatedAuthorKim, Min Hwan-
dc.contributor.affiliatedAuthorKim, Joo Hang-
dc.contributor.affiliatedAuthorKim, Eun Young-
dc.contributor.affiliatedAuthorLee, Jae Seok-
dc.contributor.affiliatedAuthorKang, Dae Ryong-
dc.rights.accessRightsfree-
dc.citation.volume84-
dc.citation.number2-
dc.citation.startPage196-
dc.citation.endPage202-
dc.identifier.bibliographicCitationLUNG CANCER, Vol.84(2) : 196-202, 2014-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Preventive Medicine and Public Health (예방의학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Thoracic and Cardiovascular Surgery (흉부외과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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