EGFR-activating mutations, DNA copy number abundance of ErbB family, and prognosis in lung adenocarcinoma
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Hsuan-Yu Chen1,2,3, Chia-Hsin Liu1,4,5,*, Ya-Hsuan Chang1,*, Sung-Liang Yu6, Bing-Ching Ho6, Chung-Ping Hsu7, Tsung-Ying Yang7, Kun-Chieh Chen7, Kuo-Hsuan Hsu7, Jeng-Sen Tseng7, Jiun-Yi Hsia7, Cheng-Yen Chuang7, Chi-Sheng Chang6, Yu-Cheng Li1, Ker-Chau Li1, Gee-Chen Chang7,8,9, Pan-Chyr Yang6,10,11
1Institute of Statistical Sciences, Academia Sinica, Taipei, Taiwan
2College of Medicine, National Taiwan University, Taipei, Taiwan
3College of Life Science, National Taiwan University, Taipei, Taiwan
4Bioinformatics Program, Taiwan International Graduate Program, Academia Sinica, Taipei, Taiwan
5Institute of Biomedical Informatics, National Yang-Ming University, Taipei, Taiwan
6Center of Genomic Medicine, National Taiwan University, Taipei, Taiwan
7Taichung Veterans General Hospital, Taichung, Taiwan
8Faculty of Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan
9Comprehensive Cancer Center, Taichung Veterans General Hospital, Taichung, Taiwan
10Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
11Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
*Chia-Hsin Liu and Ya-Hsuan Chang contributed equally as the first author
Hsuan-Yu Chen, e-mail: [email protected]
Gee-Chen Chang, e-mail: [email protected]
Keywords: lung adenocarcinoma, DNA copy number abundance, ErbB family, EGFR-activating mutation, prognosis
Received: July 07, 2015 Accepted: January 12, 2016 Published: January 27, 2016
In this study, EGFR-activating mutation status and DNA copy number abundances of members of ErbB family were measured in 261 lung adenocarcinomas. The associations between DNA copy number abundances of ErbB family, EGFR-activating mutation status, and prognosis were explored. Results showed that DNA copy number abundances of EGFR, ERBB2, ERBB3, and ERBB4 had associations with overall survival in lung adenocarcinoma with EGFR-activating mutations. In the stratification analysis, only ERBB2 showed significant discrepancy in patients carrying wild type EGFR and other members of ErbB family in patients carrying EGFR-activating mutation. This indicated that CNAs of ErbB family had effect modifications of EGFR-activating mutation status. Findings of this study demonstrate potential molecular guidance of patient management of lung adenocarcinoma with or without EGFR-activating mutations.
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