| Literature DB >> 24997986 |
Maolan Li1, Zhou Zhang2, Xiaoguang Li3, Junyi Ye4, Xiangsong Wu5, Zhujun Tan5, Chang Liu6, Baiyong Shen7, Xu-An Wang5, Wenguang Wu5, Daizhan Zhou8, Di Zhang8, Ting Wang8, Bingya Liu7, Kai Qu6, Qichen Ding5, Hao Weng5, Qian Ding5, Jiasheng Mu5, Yijun Shu5, Runfa Bao5, Yang Cao5, Peizhan Chen9, Tianyu Liu5, Lin Jiang5, Yunping Hu5, Ping Dong5, Jun Gu5, Wei Lu5, Weibin Shi5, Jianhua Lu5, Wei Gong5, Zhaohui Tang5, Yong Zhang5, Xuefeng Wang5, Y Eugene Chin10, Xiaoling Weng4, Hong Zhang4, Wei Tang11, Yonglan Zheng12, Lin He13, Hui Wang14, Yun Liu15, Yingbin Liu1.
Abstract
Individuals with gallbladder carcinoma (GBC), the most aggressive malignancy of the biliary tract, have a poor prognosis. Here we report the identification of somatic mutations for GBC in 57 tumor-normal pairs through a combination of exome sequencing and ultra-deep sequencing of cancer-related genes. The mutation pattern is defined by a dominant prevalence of C>T mutations at TCN sites. Genes with a significant frequency (false discovery rate (FDR)<0.05) of non-silent mutations include TP53 (47.1%), KRAS (7.8%) and ERBB3 (11.8%). Moreover, ErbB signaling (including EGFR, ERBB2, ERBB3, ERBB4 and their downstream genes) is the most extensively mutated pathway, affecting 36.8% (21/57) of the GBC samples. Multivariate analyses further show that cases with ErbB pathway mutations have a worse outcome (P=0.001). These findings provide insight into the somatic mutational landscape in GBC and highlight the key role of the ErbB signaling pathway in GBC pathogenesis.Entities:
Mesh：
Substances：
Year: 2014 PMID： 24997986 DOI： 10.1038/ng.3030
Source DB: PubMed Journal: Nat Genet ISSN： 1061-4036 Impact factor: 38.330