| Literature DB >> 29799009 |
Cheng Wang1,2,3, Rong Yin4, Juncheng Dai1,2, Yayun Gu1,2, Shaohua Cui5, Hongxia Ma1,2, Zhihong Zhang6, Jiaqi Huang7, Na Qin1,2, Tao Jiang1,2, Liguo Geng1,2, Meng Zhu1,2, Zhening Pu1,2, Fangzhi Du1,2, Yuzhuo Wang1,2, Jianshui Yang1,2, Liang Chen8, Qianghu Wang3, Yue Jiang1,2, Lili Dong5, Yihong Yao7, Guangfu Jin1,2, Zhibin Hu1,2, Liyan Jiang9, Lin Xu10, Hongbing Shen11,12.
Abstract
Chinese lung cancer patients have distinct epidemiologic and genomic features, highlighting the presence of specific etiologic mechanisms other than smoking. Here, we present a comprehensive genomic landscape of 149 non-small cell lung cancer (NSCLC) cases and identify 15 potential driver genes. We reveal that Chinese patients are specially characterized by not only highly clustered EGFR mutations but a mutational signature (MS3, 33.7%), that is associated with inflammatory tumor-infiltrating B lymphocytes (P = 0.001). The EGFR mutation rate is significantly increased with the proportion of the MS3 signature (P = 9.37 × 10-5). TCGA data confirm that the infiltrating B lymphocyte abundance is significantly higher in the EGFR-mutated patients (P = 0.007). Additionally, MS3-high patients carry a higher contribution of distant chromosomal rearrangements >1 Mb (P = 1.35 × 10-7), some of which result in fusions involving genes with important functions (i.e., ALK and RET). Thus, inflammatory infiltration may contribute to the accumulation of EGFR mutations, especially in never-smokers.Entities:
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Year: 2018 PMID： 29799009 PMCID： PMC5967326 DOI： 10.1038/s41467-018-04492-2
Source DB: PubMed Journal: Nat Commun ISSN： 2041-1723 Impact factor: 14.919