AKR1B10, a good prognostic indicator in gastric cancer

被引：39
作者：
Yao, H. -B. [1 ]
Xu, Y. [1 ]
Chen, L. -G. [1 ]
Guan, T. -P [1 ]
Ma, Y-Y [2 ]
He, X. -J. [2 ]
Xia, Y. -J. [2 ]
Tao, H. -Q. [2 ]
Shao, Q. -S. [1 ]
机构：
[1] Zhejiang Prov Peoples Hosp, Dept Gastrointestinal Surg, Hangzhou 310014, Zhejiang, Peoples R China
[2] Key Lab Gastroenterol Zhejiang Prov, Hangzhou 310014, Zhejiang, Peoples R China
来源：
EJSO | 2014年 / 40卷 / 03期
关键词：
AKR1B10; Gastric cancer; Metastasis; Prognosis; HUMAN ALDOSE REDUCTASE; KETO REDUCTASES; MEMBER B10; FAMILY; EXPRESSION; OVEREXPRESSION; IDENTIFICATION; 1B10; DIETARY; ALPHA;
D O I：
10.1016/j.ejso.2013.12.014
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Background and objectives: The aim of the study was to investigate the correlation between AKR1B10 expression and clinicopathological features of gastric cancer (GC). Methods: Real-time polymerase chain reaction (RT-PCR) was performed to determine AKR1B10 mRNA expression. AKR1B10 protein levels were measured by immunohistochemistry. Results: RT-PCR analysis confirmed that AKR1B10 was significantly down-regulated in gastric cancer compared with paired, normal mucosa. Immunohistochemistry revealed that the percentage of AKR1B10-positive specimens was lower in gastric carcinoma compared with normal specimens. The frequency of AKR1B10-positive GC specimens was higher in patients with tumor size <5 cm, no lymph node metastasis, no distant metastasis' and lower tumor stages The mean survival time for patients in the AKR1B10-positive group was significantly higher compared with the AKR1B1-negative group. The 5-year survival rate for the AKR1B10-positive group was also significantly higher than for the AKR1B1-negative group. Cox regression analysis revealed that AKR1B10 expression is an independent prognostic factor of GC. Conclusions: Expression of AKR1B10 in gastric cancer was significantly associated with tumor size, lymph node metastasis, distance metastasis and TNM stage, and AKR1B10 may be a good prognostic indicator in gastric cancer. (C) 2013 Elsevier Ltd. All rights reserved.
引用
收藏
页码：318 / 324
页数：7
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