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SOX2 expression is associated with FGFR fusion genes and predicts favorable outcome in lung squamous cell carcinomas

Authors Zheng S, Pan Y, Wang R, Li Y, Cheng C, Shen X, Li B, Zheng D, Sun Y, Chen H

Received 27 June 2015

Accepted for publication 10 September 2015

Published 19 October 2015 Volume 2015:8 Pages 3009—3016

DOI https://doi.org/10.2147/OTT.S91293

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Jia Fan

Peer reviewer comments 2

Editor who approved publication: Dr William Cho


Shanbo Zheng,1,2,* Yunjian Pan,1,2,* Rui Wang,1,2 Yuan Li,2,3 Chao Cheng,1,2 Xuxia Shen,2,3 Bin Li,1,2 Difan Zheng,1,2 Yihua Sun,1,2 Haiquan Chen1,2

1Department of Thoracic Surgery, Fudan University Shanghai Cancer Center, Shanghai, People’s Republic of China; 2Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, People’s Republic of China; 3Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai, People’s Republic of China

*These authors contributed equally to this work

Objectives: SOX2 is a gene that encodes for a transcription factor, which functions as an activator or suppressor of gene transcription. SOX2 amplification and overexpression have been found in various types of tumors and play important roles in cancer cells. The aim of the study was to evaluate SOX2 expression and amplification in lung squamous cell carcinomas (SCCs) and to determine the relationship with main clinicopathologic features, patient prognosis, and common driver mutations.
Materials and methods: SOX2 protein levels were measured by immunohistochemistry, while SOX2 copy numbers were measured by fluorescence in situ hybridization in resected samples from 162 Chinese lung SCC patients. All patients were also analyzed for mutations in EGFR, HER2, BRAF, PIK3CA, NFE2L2, and FGFR fusion genes. Clinical characteristics, including age, sex, smoking status, stage, relapse-free survival (RFS), and overall survival (OS), were collected.
Results: SOX2 overexpression and amplification were observed in 58.6% and 45.9% of lung SCCs. Lung SCC patients with SOX2 overexpression were significantly associated with absence of malignant tumor family history (P=0.021), FGFR fusion gene (P=0.046), longer RFS (P=0.041), and OS (P=0.025). No correlation was found between SOX2 gene amplification and main clinicopathologic features, patient prognosis, or common driver mutations.
Conclusion: SOX2 overexpression and amplification are common in lung SCCs. SOX2 overexpression was associated with FGFR fusion genes and predicted favorable outcome in lung SCCs. The underlying relationship of SOX2 and FGFR still needs further investigation.

Keywords: lung squamous cell carcinoma, SOX2 amplification, protein expression, FGFR fusion gene, prognostic marker

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