DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, June Koo | ko |
dc.contributor.author | Park, Seong Yeol | ko |
dc.contributor.author | Park, Hansol | ko |
dc.contributor.author | Kim, Sehui | ko |
dc.contributor.author | Lee, Jongkeun | ko |
dc.contributor.author | Lee, Junehawk | ko |
dc.contributor.author | Youk, Jeonghwan | ko |
dc.contributor.author | Yi, Kijong | ko |
dc.contributor.author | An, Yohan | ko |
dc.contributor.author | Park, In Kyu | ko |
dc.contributor.author | Kang, Chang Hyun | ko |
dc.contributor.author | Chung, Doo Hyun | ko |
dc.contributor.author | Kim, Tae Min | ko |
dc.contributor.author | Jeon, Yoon Kyung | ko |
dc.contributor.author | Hong, Dongwan | ko |
dc.contributor.author | Park, Peter J. | ko |
dc.contributor.author | Ju, Young Seok | ko |
dc.contributor.author | Kim, Young Tae | ko |
dc.date.accessioned | 2019-07-08T07:10:11Z | - |
dc.date.available | 2019-07-08T07:10:11Z | - |
dc.date.created | 2019-07-01 | - |
dc.date.created | 2019-07-01 | - |
dc.date.created | 2019-07-01 | - |
dc.date.created | 2019-07-01 | - |
dc.date.issued | 2019-06 | - |
dc.identifier.citation | CELL, v.177, no.7, pp.1842 - + | - |
dc.identifier.issn | 0092-8674 | - |
dc.identifier.uri | http://hdl.handle.net/10203/263092 | - |
dc.description.abstract | Mutational processes giving rise to lung adenocarcinomas (LADCs) in non-smokers remain elusive. We analyzed 138 LADC whole genomes, including 83 cases with minimal contribution of smoking-associated mutational signature. Genomic rearrangements were not correlated with smoking-associated mutations and frequently served as driver events of smoking-signature-low LADCs. Complex genomic rearrangements, including chromothripsis and chromoplexy, generated 74% of known fusion oncogenes, including EML4-ALK, CD74-ROS1, and KIF5B-RET. Unlike other collateral rearrangements, these fusion-oncogene-associated rearrangements were frequently copy-number-balanced, representing a genomic signature of early oncogenesis. Analysis of mutation timing revealed that fusions and point mutations of canonical oncogenes were often acquired in the early decades of life. During a long latency, cancer-related genes were disrupted or amplified by complex rearrangements. The genomic landscape was different between subgroups- EGFR-mutant LADCs had frequent whole-genome duplications with p53 mutations, whereas fusiononcogene-driven LADCs had frequent SETD2 mutations. Our study highlights LADC oncogenesis driven by endogenous mutational processes. | - |
dc.language | English | - |
dc.publisher | CELL PRESS | - |
dc.title | Tracing Oncogene Rearrangements in the Mutational History of Lung Adenocarcinoma | - |
dc.type | Article | - |
dc.identifier.wosid | 000471256800022 | - |
dc.identifier.scopusid | 2-s2.0-85066936967 | - |
dc.type.rims | ART | - |
dc.citation.volume | 177 | - |
dc.citation.issue | 7 | - |
dc.citation.beginningpage | 1842 | - |
dc.citation.endingpage | + | - |
dc.citation.publicationname | CELL | - |
dc.identifier.doi | 10.1016/j.cell.2019.05.013 | - |
dc.contributor.localauthor | Ju, Young Seok | - |
dc.contributor.nonIdAuthor | Kim, Sehui | - |
dc.contributor.nonIdAuthor | Lee, Jongkeun | - |
dc.contributor.nonIdAuthor | Lee, Junehawk | - |
dc.contributor.nonIdAuthor | Park, In Kyu | - |
dc.contributor.nonIdAuthor | Kang, Chang Hyun | - |
dc.contributor.nonIdAuthor | Chung, Doo Hyun | - |
dc.contributor.nonIdAuthor | Kim, Tae Min | - |
dc.contributor.nonIdAuthor | Jeon, Yoon Kyung | - |
dc.contributor.nonIdAuthor | Hong, Dongwan | - |
dc.contributor.nonIdAuthor | Park, Peter J. | - |
dc.contributor.nonIdAuthor | Kim, Young Tae | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordPlus | WHOLE-GENOME | - |
dc.subject.keywordPlus | COPY NUMBER | - |
dc.subject.keywordPlus | CANCER | - |
dc.subject.keywordPlus | EVOLUTION | - |
dc.subject.keywordPlus | GENE | - |
dc.subject.keywordPlus | CHROMOTHRIPSIS | - |
dc.subject.keywordPlus | LANDSCAPE | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | TRANSFORMATION | - |
dc.subject.keywordPlus | CRIZOTINIB | - |
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