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Meta-Analysis
. 2016 Dec 21:6:39404.
doi: 10.1038/srep39404.

Genetic polymorphisms -137 (rs187238) and -607 (rs1946518) in the interleukin-18 promoter may not be associated with development of hepatocellular carcinoma

Shao-Liang Zhu  1 , Yun Zhao  2 , Xue-Ying Hu  3 , Tao Luo  1 , Zu-Shun Chen  1 , Yu Zhang  1 , Shui-Hua Yang  4 , Lu Zhou  5 , Le-Qun Li  1
Affiliations
Meta-Analysis

Genetic polymorphisms -137 (rs187238) and -607 (rs1946518) in the interleukin-18 promoter may not be associated with development of hepatocellular carcinoma

Shao-Liang Zhu et al. Sci Rep. .

Abstract

This study meta-analyzed the literature on possible association of polymorphisms -137 (rs187238) and -607 (rs1946518) in the interleukin-18 (IL-18) promoter with risk of hepatocellular carcinoma (HCC). The analysis included 8 case-control studies on the -137 polymorphism (1,318 cases, 2,254 controls) and 7 case-control studies on the -607 polymorphism (1,262 cases, 1,696 controls). None of the five genetic models suggested a significant association between the -137 polymorphism and HCC risk: allelic model, OR 0.99, 95% CI 0.74-1.34, P = 0.97; recessive model, OR 0.98, 95% CI 0.65-1.46, P = 0.91; dominant model, OR 1.35, 95% CI 0.73-2.52, P = 0.34; homozygous model, OR 0.99, 95% CI 0.65-1.49, P = 0.95; heterozygous model, OR 0.99, 95% CI 0.66-1.48, P = 0.94. Similar results were obtained in subgroup analyses of Asian patients, Chinese patients, or patients with hepatitis B virus (HBV)-related HCC. Similar results were also obtained for the -607 polymorphism across the entire study population as well as in the three subgroups. The available evidence suggests no significant association of the -137 or -607 polymorphisms with risk of HCC in general or specifically of HBV-related HCC. These conclusions should be verified in large, well-designed studies.

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Figures

Figure 1
Figure 1. Flowchart of study selection.
HCC, hepatocellular carcinoma; LC, liver cirrhosis.
Figure 2
Figure 2. Forest plot describing the association between the -137 polymorphism (rs187238) and risk of across all study participants according to different genetic models.
(A) allelic (C-allele vs. G-allele), (B) recessive (CC vs. GC + GG), (C) dominant (GG vs. GC + CC), (D) homozygous (CC vs. GG) and (E) heterozygous (GC vs. GG).
Figure 3
Figure 3. Forest plot describing the association between the -607 polymorphism (rs1946518) and risk of hepatocellular carcinoma across all study participants according to different genetic models.
(A) allelic (C-allele vs. A-allele), (B) recessive (CC vs. AC + AA), (C) dominant (AA vs. AC + CC), (D) homozygous (CC vs. AA) and (E) heterozygous (AC vs. AA).
Figure 4
Figure 4. Begg’s funnel plot to assess publication bias in the meta-analysis of a potential association between the -137 polymorphism (rs187238) and risk of hepatocellular carcinoma across all study participants according to different genetic models.
(A) allelic (C-allele vs. G-allele), (B) recessive (CC vs. GC + GG), (C) dominant (GG vs. GC + CC), (D) homozygous (CC vs. GG) and (E) heterozygous (GC vs. GG).
Figure 5
Figure 5. Begg’s funnel plot to assess publication bias in the meta-analysis of a potential association between the -607 polymorphism (rs1946518) and risk of hepatocellular carcinoma across all study participants according to different genetic models.
(A) allelic (C-allele vs. A-allele), (B) recessive (CC vs. AC + AA), (C) dominant (AA vs. AC + CC), (D) homozygous (CC vs. AA) and (E) heterozygous (AC vs. AA).
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