Oncotarget

Research Papers:

Investigation of TCF7L2, LEP and LEPR polymorphisms with esophageal squamous cell carcinomas

Hao Qiu, Xunting Lin, Weifeng Tang, Chao Liu, Yu Chen, Hao Ding, Mingqiang Kang and Shuchen Chen _

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Oncotarget. 2017; 8:109107-109119. https://doi.org/10.18632/oncotarget.22619

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Abstract

Hao Qiu1,*, Xunting Lin2,*, Weifeng Tang3, Chao Liu3, Yu Chen4, Hao Ding5, Mingqiang Kang6,7,8 and Shuchen Chen6

1Department of Immunology, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu Province, China

2Department of Gastroenterology, Zhongshan Hospital Xiamen University, Xiamen, Fujian Province, China

3Department of Cardiothoracic Surgery, Affiliated People’s Hospital of Jiangsu University, Zhenjiang, Jiangsu Province, China

4Department of Medical Oncology, Fujian Cancer Hospital, Fujian Medical University Cancer Hospital, Fuzhou, Fujian Province, China

5Department of Respiratory Disease, Affiliated People’s Hospital of Jiangsu University, Zhenjiang, Jiangsu Province, China

6Department of Thoracic Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian Province, China

7Key Laboratory of Ministry of Education for Gastrointestinal Cancer, Fujian Medical University, Fuzhou, Fujian Province, China

8Fujian Key Laboratory of Tumor Microbiology, Fujian Medical University, Fuzhou, Fujian Province, China

*These authors have contributed equally to this work

Correspondence to:

Shuchen Chen, email: [email protected]

Keywords: TCF7L2; LEP; LEPR; polymorphism; ESCC

Received: June 05, 2017     Accepted: August 26, 2017     Published: November 17, 2017

ABSTRACT

Single nucleotide polymorphisms (SNPs) in energy metabolism related gene may be key agents in the development of human malignancies. In this study, we aimed to examine the association of transcription factor 7-like 2, Leptin (LEP) and LEP receptor (LEPR) polymorphisms with esophageal squamous cell carcinoma (ESCC). A total of 507 ESCC cases and 1,496 controls were enrolled. We found that LEPR rs6588147 AA genotype was associated with ESCC risk (AA vs. GG/GA: adjusted OR=1.90, 95%CI=1.00–3.61, P=0.049). In the stratified analyses, LEPR rs6588147 G>A polymorphism increased the risk of ESCC (<63 years subgroup: AA vs. GG: adjusted OR=2.58, 95%CI=1.00–6.62, P=0.049 and AA vs. GA/GG: adjusted OR=2.71, 95%CI=1.06–6.91, P=0.038; male subgroup: AA vs. GG: adjusted OR=2.19, 95%CI=1.02–4.67, P=0.044 and AA vs. GA/GG: adjusted OR=2.26, 95%CI=1.06–4.80, P=0.035). However, LEP rs7799039 A>G decreased the risk of ESCC (≥63 years subgroup: GG vs. AA: adjusted OR=0.47, 95%CI=0.23–0.95, P=0.035 and GG vs. AA/AG: adjusted OR=0.48, 95%CI=0.24–0.96, P=0.038; BMI≥24 kg/m2 subgroup: AG vs. AA: adjusted OR=0.66, 95%CI=0.45–0.99, P=0.044). In addition, LEPR rs1137101 G>A polymorphism decreased ESCC risk in some subgroups (ever smoking subgroup: GA vs. GG: adjusted OR=0.66, 95%CI=0.44–1.00, P=0.049; ever drinking subgroup: GA vs. GG: adjusted OR=0.54, 95%CI=0.31–0.95, P=0.031 and GA/AA vs. GG: adjusted OR=0.54, 95%CI=0.31–0.93, P=0.027). Our findings suggest that LEPR rs6588147 G>A polymorphism is associated with the increased risk of ESCC; however, LEP rs7799039 A>G and LEPR rs1137101 G>A polymorphisms may be protective factors for ESCC.


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