SynthesisScientific reports2016
Genetic polymorphisms -137 (rs187238) and -607 (rs1946518) in the interleukin-18 promoter may not be associated with development of hepatocellular carcinoma.
Synthesis in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.
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Who cites it
8 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Associations between twelve common gene polymorphisms and susceptibility to hepatocellular carcinoma: evidence from a meta-analysis.World journal of surgical oncology · 2019Pooled it
- Inflammasomes and their roles in the pathogenesis of viral hepatitis and their related complications: An updated systematic review.Immunology letters · 2019Pooled it
- Polymorphism Analysis of Interleukin-18 and Interleukin-37 Genes in Hepatitis B Infections with Different Outcomes: A Preliminary Report from an Iranian Population.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Interleukin-18 in Health and Disease.International journal of molecular sciences · 2019Review
- Investigation of NF-κB-94ins/del ATTG and CARD8 (rs2043211) Gene Polymorphism in Acute Lymphoblastic Leukemia.Frontiers in endocrinology · 2019Article
- Evaluation of the Role of -137G/C Single Nucleotide Polymorphism (rs187238) and Gene Expression Levels of the IL-18 in Patients with Coronary Artery Disease.Oman medical journal · 2018Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
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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