Lack of association between pro-inflammatory genotypes of the interleukin-1 (IL-1B -31 C/+ and IL-1RN *2/*2) and gastric cancer/duodenal ulcer in Korean population

Lee, Seong-Gene; Kim, Byung-Sik; Choi, Wook; Lee, Inchul; Choi, Jae-Won; Song, Kyuyoung

doi:10.1016/s1043-4666(03)00032-2

Cited by 67 publications

(55 citation statements)

References 18 publications

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“…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. 1).…”

Section: Resultsmentioning

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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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%

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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“…Lee et al have not confirmed an association between the polymorphism of IL1B-31 and increased risk of gastric cancer (Lee et al, 2003). Matsukara and colleagues reported that ethnic differences of IL1B gene polymorphism affect the risk of gastric atrophy.…”

Section: Discussionmentioning

confidence: 95%

Association of Cytokine Gene Polymorphisms with Gastritis in a Kazakh Population

Kulmambetova¹,

Imanbekova²,

Logvinenko³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…Moreover, Camargo et al [73], Zambon et al [74], and El-Omar et al [75] stated that polymorphisms in genes associated with the inflammatory response in the gastric mucosa, such as IL-1b, TNF-a, and IL-10, have been shown to be associated with higher risks for duodenal ulcer and gastric cancer. However, Kato et al [76], Lee et al [77], Gatti et al [78], and Kamangar et al [79] did not agree with these opinions, and Chang et al [80], in particular, indicated that mucosal inflammatory cytokines were related to gastroduodenal phenotypes, not to IL-1b genotypes, and they noted that H. pylori infection was a more important factor in the development of gastroduodenal phenotypes than IL-1b polymorphisms. PartidaRodríguez et al [81], however, reported that genotype TNF-b G/G showed a significant gene-dose effect with gastric cancer, and heat shock protein (HSP) 70-1 C/G showed significant association with both gastric cancer and duodenal ulcer.…”

Section: Endogenous Factorsmentioning

confidence: 99%

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

et al. 2011

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The coexistence of gastric cancer with duodenal ulcer has been found empirically to be rare, but why it is rare is difficult to explain satisfactorily. To elucidate this question, we carried out a literature review of the subject. The frequency with which the two diseases coexist is 0.1-1.7%, and the main factor associated with both gastric cancer and duodenal ulcer is Helicobacter pylori infection. However, there are marked differences between the disorders of hyperchlorhydria in duodenal ulcer, and hypochlorhydria in gastric cancer. The most acceptable view of the reason for the difference may be that the acquisition of H. pylori infection occurs mainly in childhood, so that the time of acquisition of atrophic gastritis may be the most important, and if atrophic gastritis is not acquired early, high levels of gastric acid may occur, and consequently acute antral gastritis and duodenal ulcer may occur in youth, whereas, in elderly individuals, persistent H. pylori infections and the early appearance of atrophic gastritis may be the causes of low gastric acid, and consequently gastric cancer may occur. In patients with duodenal ulcer, factors such as nonsteroidal anti-inflammatory drugs (NSAIDs) and dupA-H. pylori strains may contribute to preventing the early acquisition of atrophic gastritis, while acid-suppressive therapy and vascular endothelial growth factor and other entities may inhibit atrophic gastritis. In contrast, in gastric cancer, factors such as excessive salt intake, acid-suppressive therapy, polymorphisms of inflammatory cytokines, and the homB-H. pylori strain may contribute to the early acquisition of atrophic gastritis, while factors such as NSAIDs; fruits and vegetables; vitamins A, C, and E; and good nutrition may inhibit it.

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Lack of association between pro-inflammatory genotypes of the interleukin-1 (IL-1B -31 C/+ and IL-1RN 2/2) and gastric cancer/duodenal ulcer in Korean population

Cited by 67 publications

References 18 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

Association of Cytokine Gene Polymorphisms with Gastritis in a Kazakh Population

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

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