Research Papers:
Identification of FGF19 as a prognostic marker and potential driver gene of lung squamous cell carcinomas in Chinese smoking patients
PDF | HTML | Supplementary Files | How to cite
Metrics: PDF 2204 views | HTML 2493 views | ?
Abstract
Qiang Tan1,*, Fan Li2,*, Guan Wang3,*, Weiliang Xia2, Ziming Li1, Xiaomin Niu1, Wenxiang Ji1,2, Hong Yuan1,2, Qiang Xu4, Qingquan Luo1, Jie Zhang1, Shun Lu1
1Shanghai Lung Cancer Center, Lung Cancer Research Laboratory, Shanghai Chest Hospital Affiliated to Shanghai Jiao Tong University, Shanghai 200030, China
2State Key Laboratory of Oncogenes and Related Genes, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China
3Genomics Center, WuXi AppTec Co., Ltd., Shanghai 200131, China
4Jiahui International Hospital, Shanghai 200120, China
*These authors have contributed equally to this work
Correspondence to:
Shun Lu, e-mail: [email protected]
Keywords: FGF19, lung squamous cell carcinomas
Received: September 15, 2015 Accepted: January 24, 2016 Published: March 01, 2016
ABSTRACT
Comprehensive genomic characterizations of lung squamous cell carcinoma (LSCC) have been performed, but the differences between smokers (S-LSCC) and never smokers (NS-LSCC) are not clear, as NS-LSCC could be considered as a different disease from S-LSCC. In this study we delineated genomic alterations in a cohort of 21 NS-LSCC and 16 S-LSCC patients, and identified common gene mutations and amplifications as previously reported. Inclusion of more NS-LSCC patients enabled us to identify unreported S-LSCC- or NS-LSCC-specific alterations. Importantly, an amplification region containing FGF19, FGF3, FGF4 and CCND1 was found five-times more frequent in S-LSCC than in NS-LSCC. Amplification of FGF19 was validated in independent LSCC samples. Furthermore, FGF19 stimulated LSCC cell growth in vitro. These data implicate FGF19 as a potential driver gene in LSCC with clinic characteristics as smoking.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 7817