作者
Jake June-Koo Lee, Seongyeol Park, Hansol Park, Sehui Kim, Jongkeun Lee, Junehawk Lee, Jeonghwan Youk, Kijong Yi, Yohan An, In Kyu Park, Chang Hyun Kang, Doo Hyun Chung, Tae Min Kim, Yoon Kyung Jeon, Dongwan Hong, Peter J Park, Young Seok Ju, Young Tae Kim
发表日期
2019/6/13
期刊
Cell
卷号
177
期号
7
页码范围
1842-1857. e21
出版商
Elsevier
简介
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 …
学术搜索中的文章
JJK Lee, S Park, H Park, S Kim, J Lee, J Lee, J Youk… - Cell, 2019