Combined Polymorphism Analysis of Glutathione S-transferase M1/G1 and Interleukin-1B (IL-1B)/Interleukin 1-Receptor Antagonist (IL-1RN) and Gastric Cancer Risk in an Omani Arab Population

Al-Moundhri, Mansour; AlKindy, Mohamed; Al-Nabhani, Maryam; Bahrani, Bassim Al; Burney, Ikram A.; Al-Habsi, Hamdan; Ganguly, Shyam S.; Tanira, M. O. M.

doi:10.1097/mcg.0b013e31815853fa

Cited by 25 publications

(8 citation statements)

References 14 publications

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“…As a result, 53 articles were excluded as they failed to meet eligibility criteria, due to not investigating IL‐1B 31 polymorphism, or not case–control study. Of the remaining 38 publications, three were eliminated, due to reporting duplicate data 17, 18, 19. Ultimately, 37 studies from 35 publications 6, 10, 14, 15, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50 including 6108 cases and 8980 controls were included in the meta‐analysis (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Interleukin‐1B 31 C>T polymorphism combined with Helicobacter pylori‐modified gastric cancer susceptibility: evidence from 37 studies

Hua-yong

Zong³

et al. 2016

J Cellular Molecular Medi

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Gastric cancer is one of the most common malignancies worldwide. Interleukin‐1‐beta (IL‐1β) is a pro‐inflammatory cytokine and potent inhibitor of gastric acid secretion. Some studies provided evidence of the association between IL‐1B 31 polymorphism and gastric cancer risk while other studies did not. Therefore, we conducted a comprehensive meta‐analysis to reassess the association. A systematic literature search of the PubMed and EMBASE databases identified 37 studies with 6108 cases and 8980 controls for this meta‐analysis. The crude odd ratios (ORs) and the 95% confidence intervals (CIs) were calculated to evaluate the strength of the association. Meta‐regression was used to determine the major source of heterogeneity across the studies. The pooled analysis did not suggest the significant association of IL‐1B 31 C>T polymorphism with gastric cancer risk. Stratified analysis was performed by ethnicity, source of control, genotype method, and indicated a significantly increased gastric cancer risk associated with IL‐1B 31T variant in the population‐based subgroup (heterozygous model: OR = 1.22, 95% CI = 1.03–1.45). Moreover, stratified analysis by Helicobacter pylori infection status indicated that IL‐1B 31 polymorphism increased gastric cancer risk in infection‐positive subgroup (homozygous model: OR = 1.35, 95% CI = 1.02–1.78; heterozygous model: OR = 1.31, 95% CI = 1.04–1.66; recessive model: OR = 1.29, 95% CI = 1.04–1.61). The study suggested that IL‐1B 31 polymorphism might confer susceptibility to gastric cancer in the presence of H. pylori infection, indicating a gene–environment interaction in gastric carcinogenesis.

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Section: Resultsmentioning

confidence: 99%

“…A total of 35 articles with cases and controls were pooled together in the current meta-analysis. Two articles [17,19] included in the meta-analysis by He et al were not selected for our study because of overlapped participants. Finally, a total of 12 new studies were supplemented to our meta-analysis, when compared to the latter one.…”

Section: Discussionmentioning

confidence: 99%

Interleukin‐1B 31 C>T polymorphism combined with Helicobacter pylori‐modified gastric cancer susceptibility: evidence from 37 studies

Hua-yong

Zong³

et al. 2016

J Cellular Molecular Medi

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“…Additionally, we here could show that both the DNA methylation and gene expression profile of another key player of the interleukin signaling pathway, interleukin 1 receptor antagonist (IL1RN), is altered in T-PLL. IL1RN has also been shown to be involved in tumorigenesis in numerous tumor entities [53], [54], [55], [56].…”

Section: Discussionmentioning

confidence: 99%

A Comprehensive Microarray-Based DNA Methylation Study of 367 Hematological Neoplasms

et al. 2009

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BackgroundAlterations in the DNA methylation pattern are a hallmark of leukemias and lymphomas. However, most epigenetic studies in hematologic neoplasms (HNs) have focused either on the analysis of few candidate genes or many genes and few HN entities, and comprehensive studies are required.Methodology/Principal FindingsHere, we report for the first time a microarray-based DNA methylation study of 767 genes in 367 HNs diagnosed with 16 of the most representative B-cell (n = 203), T-cell (n = 30), and myeloid (n = 134) neoplasias, as well as 37 samples from different cell types of the hematopoietic system. Using appropriate controls of B-, T-, or myeloid cellular origin, we identified a total of 220 genes hypermethylated in at least one HN entity. In general, promoter hypermethylation was more frequent in lymphoid malignancies than in myeloid malignancies, being germinal center mature B-cell lymphomas as well as B and T precursor lymphoid neoplasias those entities with highest frequency of gene-associated DNA hypermethylation. We also observed a significant correlation between the number of hypermethylated and hypomethylated genes in several mature B-cell neoplasias, but not in precursor B- and T-cell leukemias. Most of the genes becoming hypermethylated contained promoters with high CpG content, and a significant fraction of them are targets of the polycomb repressor complex. Interestingly, T-cell prolymphocytic leukemias show low levels of DNA hypermethylation and a comparatively large number of hypomethylated genes, many of them showing an increased gene expression.Conclusions/SignificanceWe have characterized the DNA methylation profile of a wide range of different HNs entities. As well as identifying genes showing aberrant DNA methylation in certain HN subtypes, we also detected six genes—DBC1, DIO3, FZD9, HS3ST2, MOS, and MYOD1—that were significantly hypermethylated in B-cell, T-cell, and myeloid malignancies. These might therefore play an important role in the development of different HNs.

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“…found no overall associations between IL‐1B or IL‐1RN polymorphisms and predisposition to gastric cancer 47 . Ever since 2006, the zeal has remained for the elucidation of the influence of IL‐1B and IL‐1RN polymorphisms on the development of gastric cancer 36–45 …”

Section: Introductionmentioning

confidence: 99%

“…47 Ever since 2006, the zeal has remained for the elucidation of the influence of IL-1B and IL-1RN polymorphisms on the development of gastric cancer. [36][37][38][39][40][41][42][43][44][45] Accordingly, the aim of our meta-analysis was to shed more light on the role of those polymorphisms in the susceptibility to gastric carcinoma and to identify possible sources of heterogeneity among the eligible studies.…”

Section: Introductionmentioning

confidence: 99%

Interleukin‐1B and interleukin‐1 RN polymorphisms and gastric carcinoma risk: A meta‐analysis

Han

Lin

et al. 2010

J of Gastro and Hepatol

112

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Background and Aim: We aimed to explore the role of interleukin (IL)-1B cluster gene polymorphisms at positions -511, -31, and +3954 and the receptor IL-1RN variable number tandem repeat polymorphisms in the susceptibility to gastric carcinoma through a systematic review and meta-analysis. Methods: Each initially included article was scored for quality appraisal. The desirable data were extracted and registered into databases. Studies that deviated from HardyWeinberg equilibrium were excluded. Eighteen studies were ultimately eligible for the meta-analysis of IL1B-511, 21 studies for IL1B-31, 10 studies for IL1B+3954, and 20 studies for IL1RN variable number tandem repeat genetic polymorphisms, respectively. Original groups were collapsed and re-grouping was adopted in line with the most probably appropriate genetic models. Potential sources of heterogeneity were sought out via stratification and sensitivity analyses, and biases across studies were estimated. Results: The pooled odds ratios (95% confidence intervals, P-value) associated with IL-1B -511 T carriers versus CC genotypes and with RN *2 carriers versus L/L were 1.23 (1.04-1.45, P = 0.015) and 1.26 (1.06-1.51, P = 0.010), respectively, for overall gastric carcinoma; 1.31 (1.04-1.64, P = 0.020) and 1.47 (1.21-1.79, P = 0.000), respectively, for non-cardia gastric cancer; 1.55 (1.05-2.28, P = 0.026) and 1.66 (1.23-2.25, P = 0.001), respectively, for intestinal type gastric carcinoma; and 1.33 (1.04-1.71, P = 0.023) and 1.31 (1.07-1.61, P = 0.010), respectively, in Caucasians for overall gastric carcinoma. The pooled odds ratio (95% confidence interval, P-value) regarding IL-1B-31 CC plus TT versus CT was 0.73 (0.60-0.89, P = 0.002) for intestinal type gastric carcinoma. Genotyping methods and publication time could constitute the sources of heterogeneity across studies. Publication biases were not found. Conclusion: IL-1B -511 T allele and IL-1 RN *2 VNTR are significantly associated with an increased risk of developing gastric carcinoma and even more significantly with noncardia gastric carcinoma or with intestinal-type gastric carcinoma. Both are significantly associated with an increased risk of developing gastric carcinoma among Caucasians, but not among Asians or Hispanics.

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Combined Polymorphism Analysis of Glutathione S-transferase M1/G1 and Interleukin-1B (IL-1B)/Interleukin 1-Receptor Antagonist (IL-1RN) and Gastric Cancer Risk in an Omani Arab Population

Abstract: The current study suggests that the individual variation in both the cellular inflammatory modulator IL-1RN and the antioxidative property of GSTM1 may predispose individuals to an increased risk of gastric cancer.

Cited by 25 publications

References 14 publications

Interleukin‐1B 31 C>T polymorphism combined with Helicobacter pylori‐modified gastric cancer susceptibility: evidence from 37 studies

Interleukin‐1B 31 C>T polymorphism combined with Helicobacter pylori‐modified gastric cancer susceptibility: evidence from 37 studies

A Comprehensive Microarray-Based DNA Methylation Study of 367 Hematological Neoplasms

Interleukin‐1B and interleukin‐1 RN polymorphisms and gastric carcinoma risk: A meta‐analysis

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