Leptin rs7799039 (G2548A) polymorphism is associated with cancer risk: a meta-analysis involving 25,799 subjects
Authors Tang W, Kang M, Liu C, Qiu H
Received 8 October 2018
Accepted for publication 7 March 2019
Published 16 April 2019 Volume 2019:12 Pages 2879—2890
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Ru Chen
Peer reviewer comments 2
Editor who approved publication: Dr Arseniy Yuzhalin
Weifeng Tang,1 Mingqiang Kang,2–4 Chao Liu,1 Hao Qiu5
1Department of Cardiothoracic Surgery, Affiliated People’s Hospital of Jiangsu University, Zhenjiang, Jiangsu Province, People’s Republic of China; 2Department of Thoracic Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian Province, People’s Republic of China; 3Key Laboratory of Ministry of Education for Gastrointestinal Cancer, Fujian Medical University, Fuzhou, Fujian Province, People’s Republic of China; 4Fujian Key Laboratory of Tumor Microbiology, Fujian Medical University, Fuzhou, Fujian Province, People’s Republic of China; 5Department of Immunology, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu Province, People’s Republic of China
Background: Leptin (LEP) is a human analogous form of the mouse obese gene and plays a critical role in energy expenditure as well as the progression of carcinogenesis. Many studies exploring the relationship between the LEP rs7799039 (G2548A) polymorphism and cancer risk have observed controversial results. To extensively evaluate this potential association, we conducted this meta-analysis.
Methods: All eligible studies published up to August 2018 on the relationship between the LEP rs7799039 G>A polymorphism and cancer risk were obtained by searching PubMed, EMBASE, and the China Biology Medicine databases. The association of LEP rs7799039 G>A polymorphism with cancer risk was evaluated by crude ORs together with their 95% CI’s.
Results: Thirty-one case–control studies involving 25,799 subjects were included for meta-analysis. We identify a significant correlation with an overall cancer risk when these eligible case–control studies were pooled for analysis: for AA vs GG: an OR = 1.22, 95% CI = 1.01–1.48, P = 0.042 and for AA/GA vs GG: an OR = 1.16, 95% CI = 1.02–1.33, P = 0.026. A significant association was also detected in Asians, prostate cancer, other cancers, and hematopoietic malignancy subgroups. Sensitivity analysis was conducted by deleting an individual study in turn and calculation of the pooled ORs and CIs of the remainders. The results of sensitivity analyses indicated that no eligible study influenced the pooled ORs and CIs materially. Begg’s and Egger’s tests revealed that there was no evidence of publication bias.
Conclusion: In conclusion, our study suggests that the LEP rs7799039 G>A polymorphism might contribute to the development of cancer. In order to further verify or refute our findings, large and well-designed epidemiological studies are needed.
Keywords: leptin, polymorphism, cancer, risk, energy, meta-analysis
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