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Published in: Journal of Experimental & Clinical Cancer Research 1/2015

Open Access 01-12-2015 | Research

Phosphorylated AKT1 is associated with poor prognosis in esophageal squamous cell carcinoma

Authors: Zhengfei Zhu, Weiwei Yu, Xiaolong Fu, Menghong Sun, Qiao Wei, Dali Li, Haiquan Chen, Jiaqing Xiang, Hecheng Li, Yawei Zhang, Weixin Zhao, Kuaile Zhao

Published in: Journal of Experimental & Clinical Cancer Research | Issue 1/2015

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Abstract

Background

The epidermal growth factor receptor (EGFR) signaling pathway is important in regulating biological behaviors in many malignancies. We explored whether expression and activation of EGFR and several components on its downstream pathways have prognostic significance in patients with esophageal squamous cell carcinoma (ESCC).

Methods

Expression of EGFR, phosphorylated (p)-EGFR, AKT1, p-AKT1, AKT2, p-AKT2, ERK1, ERK2, p-ERK1/2, STAT3, and p-STAT3 was assessed by immunohistochemical analysis of tissue microarrays for 275 ESCC patients who had undergone complete three-field lymphadenectomy. Spearman rank correlation tests were used to determine the relationships among protein expression, and Cox regression analyses were performed to determine the prognostic factors on overall survival (OS).

Results

p-EGFR expression was correlated statistically with all of the other phosphorylated markers. Gender, N stage, and p-AKT1 expression were found to be independent prognostic factors for OS. Increased expression of p-AKT1 was associated with decreased patient survival. EGFR and p-EGFR expression was not significantly associated with patient survival.

Conclusion

Activation of AKT1 was associated with poor prognosis in ESCC.
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Metadata
Title
Phosphorylated AKT1 is associated with poor prognosis in esophageal squamous cell carcinoma
Authors
Zhengfei Zhu
Weiwei Yu
Xiaolong Fu
Menghong Sun
Qiao Wei
Dali Li
Haiquan Chen
Jiaqing Xiang
Hecheng Li
Yawei Zhang
Weixin Zhao
Kuaile Zhao
Publication date
01-12-2015
Publisher
BioMed Central
Published in
Journal of Experimental & Clinical Cancer Research / Issue 1/2015
Electronic ISSN: 1756-9966
DOI
https://doi.org/10.1186/s13046-015-0212-z

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