Cited 31 times in

Identification of somatic mutations in EGFR/KRAS/ALK-negative lung adenocarcinoma in never-smokers

DC Field Value Language
dc.contributor.author장준-
dc.contributor.author정경영-
dc.contributor.author김대준-
dc.contributor.author정지예-
dc.contributor.author김세규-
dc.contributor.author조병철-
dc.contributor.author김은영-
dc.contributor.author김주항-
dc.contributor.author김한상-
dc.contributor.author김혜련-
dc.contributor.author배미경-
dc.contributor.author심효섭-
dc.contributor.author이민구-
dc.contributor.author이지현-
dc.contributor.author이진구-
dc.contributor.author이창영-
dc.date.accessioned2015-01-06T17:03:57Z-
dc.date.available2015-01-06T17:03:57Z-
dc.date.issued2014-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/99288-
dc.description.abstractBACKGROUND:Lung adenocarcinoma is a highly heterogeneous disease with various etiologies, prognoses, and responses to therapy. Although genome-scale characterization of lung adenocarcinoma has been performed, a comprehensive somatic mutation analysis of EGFR/KRAS/ALK-negative lung adenocarcinoma in never-smokers has not been conducted. METHODS:We analyzed whole exome sequencing data from 16 EGFR/KRAS/ALK-negative lung adenocarcinomas and additional 54 tumors in two expansion cohort sets. Candidate loci were validated by target capture and Sanger sequencing. Gene set analysis was performed using Ingenuity Pathway Analysis. RESULTS:We identified 27 genes potentially implicated in the pathogenesis of lung adenocarcinoma. These included targetable genes involved in PI3K/mTOR signaling (TSC1, PIK3CA, AKT2) and receptor tyrosine kinase signaling (ERBB4) and genes not previously highlighted in lung adenocarcinomas, such as SETD2 and PBRM1 (chromatin remodeling), CHEK2 and CDC27 (cell cycle), CUL3 and SOD2 (oxidative stress), and CSMD3 and TFG (immune response). In the expansion cohort (N = 70), TP53 was the most frequently altered gene (11%), followed by SETD2 (6%), CSMD3 (6%), ERBB2 (6%), and CDH10 (4%). In pathway analysis, the majority of altered genes were involved in cell cycle/DNA repair (P <0.001) and cAMP-dependent protein kinase signaling (P <0.001). CONCLUSIONS:The genomic makeup of EGFR/KRAS/ALK-negative lung adenocarcinomas in never-smokers is remarkably diverse. Genes involved in cell cycle regulation/DNA repair are implicated in tumorigenesis and represent potential therapeutic targets.-
dc.description.statementOfResponsibilityopen-
dc.format.extent1~10-
dc.relation.isPartOfGENOME MEDICINE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleIdentification of somatic mutations in EGFR/KRAS/ALK-negative lung adenocarcinoma in never-smokers-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorJin Woo Ahn-
dc.contributor.googleauthorHan Sang Kim-
dc.contributor.googleauthorJung-Ki Yoon-
dc.contributor.googleauthorHoon Jang-
dc.contributor.googleauthorSoo Min Han-
dc.contributor.googleauthorSungho Eun-
dc.contributor.googleauthorHyo Sup Shim-
dc.contributor.googleauthorHyun-Jung Kim-
dc.contributor.googleauthorDae Joon Kim-
dc.contributor.googleauthorJin Gu Lee-
dc.contributor.googleauthorChang Young Lee-
dc.contributor.googleauthorMi Kyung Bae-
dc.contributor.googleauthorKyung Young Chung-
dc.contributor.googleauthorJi Ye Jung-
dc.contributor.googleauthorEun Young Kim-
dc.contributor.googleauthorSe Kyu Kim-
dc.contributor.googleauthorJoon Chang-
dc.contributor.googleauthorHye Ryun Kim-
dc.contributor.googleauthorJoo Hang Kim-
dc.contributor.googleauthorMin Goo Lee-
dc.contributor.googleauthorByoung Chul Cho-
dc.contributor.googleauthorJi Hyun Lee-
dc.contributor.googleauthorDuhee Bang-
dc.identifier.doi10.1186/gm535-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA03472-
dc.contributor.localIdA03571-
dc.contributor.localIdA00368-
dc.contributor.localIdA03735-
dc.contributor.localIdA00602-
dc.contributor.localIdA03822-
dc.contributor.localIdA00945-
dc.contributor.localIdA01166-
dc.contributor.localIdA01792-
dc.contributor.localIdA02219-
dc.contributor.localIdA02781-
dc.contributor.localIdA03225-
dc.contributor.localIdA03245-
dc.contributor.localIdA00811-
dc.contributor.localIdA03214-
dc.contributor.localIdA01098-
dc.relation.journalcodeJ00938-
dc.identifier.eissn1756-994X-
dc.identifier.pmid24576404-
dc.contributor.alternativeNameChang, Joon-
dc.contributor.alternativeNameChung, Kyung Young-
dc.contributor.alternativeNameKim, Dae Joon-
dc.contributor.alternativeNameJung, Ji Ye-
dc.contributor.alternativeNameKim, Se Kyu-
dc.contributor.alternativeNameCho, Byoung Chul-
dc.contributor.alternativeNameKim, Eun Young-
dc.contributor.alternativeNameKim, Joo Hang-
dc.contributor.alternativeNameKim, Han Sang-
dc.contributor.alternativeNameKim, Hye Ryun-
dc.contributor.alternativeNameBae, Mi Kyung-
dc.contributor.alternativeNameShim, Hyo Sup-
dc.contributor.alternativeNameLee, Min Goo-
dc.contributor.alternativeNameLee, Ji Hyun-
dc.contributor.alternativeNameLee, Jin Gu-
dc.contributor.alternativeNameLee, Chang Young-
dc.contributor.affiliatedAuthorChang, Joon-
dc.contributor.affiliatedAuthorChung, Kyung Young-
dc.contributor.affiliatedAuthorKim, Dae Joon-
dc.contributor.affiliatedAuthorJung, Ji Ye-
dc.contributor.affiliatedAuthorKim, Se Kyu-
dc.contributor.affiliatedAuthorCho, Byoung Chul-
dc.contributor.affiliatedAuthorKim, Joo Hang-
dc.contributor.affiliatedAuthorKim, Hye Ryun-
dc.contributor.affiliatedAuthorBae, Mi Kyung-
dc.contributor.affiliatedAuthorShim, Hyo Sup-
dc.contributor.affiliatedAuthorLee, Min Goo-
dc.contributor.affiliatedAuthorLee, Jin Gu-
dc.contributor.affiliatedAuthorLee, Chang Young-
dc.contributor.affiliatedAuthorKim, Eun Young-
dc.contributor.affiliatedAuthorLee, Ji Hyun-
dc.contributor.affiliatedAuthorKim, Han Sang-
dc.citation.volume6-
dc.citation.number18-
dc.citation.startPage1-
dc.citation.endPage10-
dc.identifier.bibliographicCitationGENOME MEDICINE, Vol.6(18) : 1-10, 2014-
dc.identifier.rimsid55983-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Thoracic and Cardiovascular Surgery (흉부외과학교실) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers

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