Cited 40 times in
Prediction for response duration to epidermal growth factor receptor-tyrosine kinase inhibitors in EGFR mutated never smoker lung adenocarcinoma
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 조병철 | - |
dc.contributor.author | 김대준 | - |
dc.contributor.author | 김세규 | - |
dc.contributor.author | 김주항 | - |
dc.contributor.author | 김혜련 | - |
dc.contributor.author | 심효섭 | - |
dc.contributor.author | 임선민 | - |
dc.contributor.author | 장준 | - |
dc.date.accessioned | 2015-01-06T16:34:20Z | - |
dc.date.available | 2015-01-06T16:34:20Z | - |
dc.date.issued | 2014 | - |
dc.identifier.issn | 0169-5002 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/98356 | - |
dc.description.abstract | OBJECTIVES: 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.statementOfResponsibility | open | - |
dc.format.extent | 374~382 | - |
dc.relation.isPartOf | LUNG CANCER | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Adenocarcinoma/diagnosis* | - |
dc.subject.MESH | Adenocarcinoma/drug therapy | - |
dc.subject.MESH | Adenocarcinoma/mortality | - |
dc.subject.MESH | Adult | - |
dc.subject.MESH | Aged | - |
dc.subject.MESH | Class I Phosphatidylinositol 3-Kinases | - |
dc.subject.MESH | DNA Mutational Analysis | - |
dc.subject.MESH | Drug Resistance, Neoplasm/genetics | - |
dc.subject.MESH | Female | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Lung/diagnostic imaging | - |
dc.subject.MESH | Lung/drug effects* | - |
dc.subject.MESH | Lung/pathology | - |
dc.subject.MESH | Lung Neoplasms/diagnosis* | - |
dc.subject.MESH | Lung Neoplasms/drug therapy* | - |
dc.subject.MESH | Lung Neoplasms/mortality | - |
dc.subject.MESH | Male | - |
dc.subject.MESH | Middle Aged | - |
dc.subject.MESH | Mutation/genetics | - |
dc.subject.MESH | Oncogene Protein v-akt/genetics | - |
dc.subject.MESH | PTEN Phosphohydrolase/genetics | - |
dc.subject.MESH | Phosphatidylinositol 3-Kinases/genetics | - |
dc.subject.MESH | Prognosis | - |
dc.subject.MESH | Protein Kinase Inhibitors/therapeutic use* | - |
dc.subject.MESH | Protein-Serine-Threonine Kinases/genetics | - |
dc.subject.MESH | Radiography | - |
dc.subject.MESH | Receptor, Epidermal Growth Factor/antagonists & inhibitors | - |
dc.subject.MESH | Receptor, Epidermal Growth Factor/genetics | - |
dc.subject.MESH | Smoking | - |
dc.subject.MESH | Survival Analysis | - |
dc.subject.MESH | Treatment Outcome | - |
dc.subject.MESH | Tumor Burden/drug effects | - |
dc.title | Prediction for response duration to epidermal growth factor receptor-tyrosine kinase inhibitors in EGFR mutated never smoker lung adenocarcinoma | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Thoracic & Cardiovascular Surgery (흉부외과학) | - |
dc.contributor.googleauthor | Hye Ryun Kim | - |
dc.contributor.googleauthor | Byoung Chul Cho | - |
dc.contributor.googleauthor | Hyo Sup Shim | - |
dc.contributor.googleauthor | Sun Min Lim | - |
dc.contributor.googleauthor | Se Kyu Kim | - |
dc.contributor.googleauthor | Joon Chang | - |
dc.contributor.googleauthor | Dae Joon Kim | - |
dc.contributor.googleauthor | Joo Hang Kim | - |
dc.identifier.doi | 10.1016/j.lungcan.2013.12.011 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A03822 | - |
dc.contributor.localId | A00368 | - |
dc.contributor.localId | A00602 | - |
dc.contributor.localId | A00945 | - |
dc.contributor.localId | A01166 | - |
dc.contributor.localId | A02219 | - |
dc.contributor.localId | A03369 | - |
dc.contributor.localId | A03472 | - |
dc.relation.journalcode | J02174 | - |
dc.identifier.eissn | 1872-8332 | - |
dc.identifier.pmid | 24468202 | - |
dc.identifier.url | http://www.sciencedirect.com/science/article/pii/S0169500213005813 | - |
dc.subject.keyword | AKT1, 2 | - |
dc.subject.keyword | EGFR | - |
dc.subject.keyword | Lung adenocarcinoma | - |
dc.subject.keyword | PI3KCA | - |
dc.subject.keyword | PTEN | - |
dc.subject.keyword | Response to EGFR TKIs | - |
dc.subject.keyword | STK11 mutations | - |
dc.contributor.alternativeName | Cho, Byoung Chul | - |
dc.contributor.alternativeName | Kim, Dae Joon | - |
dc.contributor.alternativeName | Kim, Se Kyu | - |
dc.contributor.alternativeName | Kim, Joo Hang | - |
dc.contributor.alternativeName | Kim, Hye Ryun | - |
dc.contributor.alternativeName | Shim, Hyo Sup | - |
dc.contributor.alternativeName | Lim, Sun Min | - |
dc.contributor.alternativeName | Chang, Joon | - |
dc.contributor.affiliatedAuthor | Cho, Byoung Chul | - |
dc.contributor.affiliatedAuthor | Kim, Dae Joon | - |
dc.contributor.affiliatedAuthor | Kim, Se Kyu | - |
dc.contributor.affiliatedAuthor | Kim, Joo Hang | - |
dc.contributor.affiliatedAuthor | Kim, Hye Ryun | - |
dc.contributor.affiliatedAuthor | Shim, Hyo Sup | - |
dc.contributor.affiliatedAuthor | Lim, Sun Min | - |
dc.contributor.affiliatedAuthor | Chang, Joon | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 83 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 374 | - |
dc.citation.endPage | 382 | - |
dc.identifier.bibliographicCitation | LUNG CANCER, Vol.83(3) : 374-382, 2014 | - |
dc.identifier.rimsid | 56550 | - |
dc.type.rims | ART | - |
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