Leptin receptor Gln223Arg and Lys109Arg polymorphisms may be associated with HBV‐related hepatocellular carcinoma risk: A system review and meta‐analysis

Author:

Dong Xiaofeng1,Zou Mengjie2,Li Chunxing3,Luo Honglin4,Zhu Shaoliang1ORCID,Gong Zheng5

Affiliation:

1. Department of Hepatobiliary, Pancreas and Spleen Surgery, The People's Hospital of Guangxi Zhuang Autonomous Region Guangxi Academy of Medical Sciences Nanning China

2. Department of Nephrology, The People's Hospital of Guangxi Zhuang Autonomous Region Guangxi Academy of Medical Sciences Nanning China

3. Department of Operating Room, The People's Hospital of Guangxi Zhuang Autonomous Region Guangxi Academy of Medical Sciences Nanning China

4. Institute of Oncology, The People's Hospital of Guangxi Zhuang Autonomous Region Guangxi Academy of Medical Sciences Nanning China

5. Department of Anesthesiology, The People's Hospital of Guangxi Zhuang Autonomous Region Guangxi Academy of Medical Sciences Nanning China

Abstract

AbstractIncreasing evidence has suggested a strong association of hepatocellular carcinoma (HCC) susceptibility and Gln223Arg (rs1137101) and Lys109Arg (rs1137100) polymorphisms in leptin receptor (LEPR) genes. To provide a quantitative assessment for such correlation, we reviewed all related systems and conducted meta‐analysis for case and control researches. A literature search of Web of Science, EMBASE, PubMed, Scopus as well as China National Knowledge Infrastructure databases was collected. 95% confidence intervals (95% CIs) together with odds ratios (ORs) were calculated. Five case–control researches consisting of 1323 cases and 1919 control cases were incorporated into meta‐analysis. Researches indicated A‐allelic and AA genotype of rs1137101 were substantially related to boosted susceptibility of hepatitis B virus (HBV)‐related HCC (mutant model, OR = 1.81, 95% CI = 1.36–2.41, p < .001; allelic model, OR = 1.55, 95% CI = 1.32–1.83, p < .001). On the contrary, we observed GG genotype of rs1137101 substantially related to reduced risk of HBV‐related HCC (wild model, OR 0.59, 95%CI = 0.46–0.75, p < .001). We observed AA genotype of rs1137100 relevant to boosted HCC risk (mutant model, OR = 1.51, 95%CI = 1.14–2.01, p = .005) as well as in those with HBV‐related HCCs (homozygous model, OR = 2.12, 95%CI = 1.49–3.02, p < .001; mutant model, OR = 1.67, 95%CI = 1.23–2.26, p = .001). G‐allele and AA genotype of rs1137101 might be in connection with boosted HBV‐related HCC susceptibility, and wild‐type GG genotype might prevent diseases. AA genotype of rs1137100 might also improve HBV‐related HCC susceptibility. Such conclusions ought to be validated by larger and better‐designed researches.

Publisher

Wiley

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