Predictive value of EGFR overexpression and gene amplification on icotinib efficacy in patients with advanced esophageal squamous cell carcinoma
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Xi Wang1,*, Haitao Niu2,*, Qingxia Fan3, Ping Lu4, Changwu Ma5, Wei Liu6, Ying Liu7, Weiwei Li4, Shaoxuan Hu1, Yun Ling8, Lei Guo8, Jianming Ying8, Jing Huang1
1Department of Medical Oncology, Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College (CAMS & PUMC), Beijing, China
2Department of VIP Medical Oncology, Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College (CAMS & PUMC), Beijing, China
3Department of Medical Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China
4Department of Medical Oncology, The First Affiliated Hospital of Xinxiang Medical College, Xinxiang, Henan, China
5Department of Medical Oncology, Chifeng City People's Hospital, Chengfeng, Inner Mongolia, China
6Department of Medical Oncology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China
7Department of Medical Oncology, Cancer Hospital of Henan Province, Zhengzhou, Henan, China
8Department of Pathology, Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College (CAMS & PUMC), Beijing, China
*These authors have contributed equally to this work
Jing Huang, e-mail: firstname.lastname@example.org
Jianming Ying, e-mail: email@example.com
Keywords: EGFR, overexpression, amplification, icotinib, esophageal cancer
Received: January 29, 2016 Accepted: March 07, 2016 Published: March 22, 2016
This study aimed to search for a molecular marker for targeted epithelial growth factor receptor (EGFR) inhibitor Icotinib by analyzing protein expression and amplification of EGFR proto-oncogene in esophageal squamous cell carcinoma (ESCC) patients.
Immunohistochemistry and fluorescence in situ hybridization (FISH) was used to assess EGFR expression and gene amplification status in 193 patients with ESCC. We also examined the association between EGFR overexpression and the efficacy of a novel EGFR TKI, icotinib, in 62 ESCC patients.
Of the 193 patients, 95 (49.2%) patients showed EGFR overexpression (3+), and 47(24.4%) patients harbored EGFR FISH positivity. EGFR overexpression was significantly correlated with clinical stage and lymph node metastasis (p<0.05). In addition, EGFR overexpression was significantly correlated with EGFR FISH positivity (p<0.001). Among the 62 patients who received icotinib, the response rate was 17.6% for patients with high EGFR-expressing tumors, which was markedly higher than the rate (0%) for patients with low to moderate EGFR-expressing tumors (p=0.341). Furthermore, all cases responded to icotinib showed EGFR overexpression.
In conclusion, our study suggests that EGFR overexpression might potentially be used in predicting the efficacy in patients treated with Icotinib. These data have implications for both clinical trial design and therapeutic strategies.
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