A Meta-Analysis of Interleukin-10 -592 Promoter Polymorphism Associated with Gastric Cancer Risk

Han, Xue; Wang, Yingchao; Li, Bing; An, Jianfu; Chen, Lu; Chen, Jinxian; Fang, Jing‐Yuan

doi:10.1371/journal.pone.0039868

Cited by 54 publications

(23 citation statements)

References 81 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Other cytokines which might bear functional relevance of defined haplotypes include IL10 [127,128], TNFα [125,129] and IL8 [130,131,132]. In most cases (except IL10 ), these cytokine polymorphisms result in a higher secretion of the corresponding cytokine leading to a stronger Th1-dominant immune response.…”

Section: Host-related Factorsmentioning

confidence: 99%

“…A meta-analysis of 18 studies on polymorphisms in the IL8 gene revealed an overall increased risk, but this was particularly remarkable in Asian populations [132]. In contrast, polymorphisms of the IL10 gene seem to have a mainly protective effect concerning gastric cancer development, especially in Asian populations [128]. There is also interaction with other risk factors like H. pylori infection or smoking tobacco [133].…”

Section: Host-related Factorsmentioning

confidence: 99%

See 1 more Smart Citation

Helicobacter pylori and Gastric Cancer

Bornschein

Malfertheiner

2014

Dig Dis

View full text Add to dashboard Cite

Infection with Helicobacter pylori is established as the major risk factor for gastric cancer development. Damage of the mucosal barrier due to H. pylori-induced inflammation enhances the carcinogenic effect of other risk factors such as salt intake or tobacco smoking. The genetic disposition of both the bacterial strain and the host can increase the potential towards gastric cancer formation. Genetic variance of the bacterial proteins CagA and VacA is associated with a higher gastric cancer risk, as are polymorphisms and epigenetic changes in host gene coding for interleukins (IL1β, IL8), transcription factors (CDX2, RUNX3) and DNA repair enzymes. Application of high-throughput assays for genome-wide assessment of either genetic structural variance or gene expression patterns may lead to a better understanding of the pathobiological background of these processes, including the underlying signaling pathways. Understanding of the stepwise alterations that take place in the transition from chronic atrophic gastritis, via metaplastic changes, to invasive neoplasia is vital to define the ‘point of no return' before which eradication of H. pylori has the potential to prevent gastric cancer. Currently, eradication as preventive strategy is only recommended for high-incidence regions in Asia; large population studies with an adequate follow-up are required to demonstrate the effectiveness of such an approach in Western populations.

show abstract

Section: Host-related Factorsmentioning

confidence: 99%

Section: Host-related Factorsmentioning

confidence: 99%

Helicobacter pylori and Gastric Cancer

Bornschein

Malfertheiner

2014

Dig Dis

View full text Add to dashboard Cite

show abstract

“…An IL-8 promoter polymorphism (IL-8-251A/T), which causes increased expression of IL-8, has been reported to be associated with progression of gastric atrophy in patients with H. pylori infection, thus increasing the risk of gastric ulcer and gastric cancer (199), as confirmed by a recent meta-analysis (200). The association of this IL-8 polymorphism with the risk of gastric cancer varies according to histological type, tumor location, H. pylori infection, and ethnicity/country (201, 202).…”

Section: Part 3 – the Immune Response Against H Pylori: Role In Cancmentioning

confidence: 88%

Helicobacter pylori CagA: From Pathogenic Mechanisms to Its Use as an Anti-Cancer Vaccine

Stein¹,

Ruggiero²,

Rappuoli³

et al. 2013

Front. Immunol.

View full text Add to dashboard Cite

Helicobacter pylori colonizes the gastric mucosa of more than 50% of the human population, causing chronic inflammation, which however is largely asymptomatic. Nevertheless, H. pylori-infected subjects can develop chronic gastritis, peptic ulcer, gastric mucosa-associated lymphoid tissue lymphoma, and gastric cancer. Chronic exposure to the pathogen and its ability to induce epithelial to mesenchymal transition (EMT) through the injection of cytotoxin-associated gene A into gastric epithelial cells may be key triggers of carcinogenesis. By deregulating cell–cell and cell–matrix interactions as well as DNA methylation, histone modifications, expression of micro RNAs, and resistance to apoptosis, EMT can actively contribute to early stages of the cancer formation. Host response to the infection significantly contributes to disease development and the concomitance of particular genotypes of both pathogen and host may turn into the most severe outcomes. T regulatory cells (Treg) have been recently demonstrated to play an important role in H. pylori-related disease development and at the same time the Treg-induced tolerance has been proposed as a possible mechanism that leads to less severe disease. Efficacy of antibiotic therapies of H. pylori infection has significantly dropped. Unfortunately, no vaccine against H. pylori is currently licensed, and protective immunity mechanisms against H. pylori are only partially understood. In spite of promising results obtained in animal models of infection with a number of vaccine candidates, few clinical trials have been conducted so far and with no satisfactory outcomes. However, prophylactic vaccination may be the only means to efficiently prevent H. pylori-associated cancers.

show abstract

“…Three polymorphisms in this gene have been connected with altered risk of gastric cancer development. Meta-analyses have revealed that the IL-10-592 AA 112 and IL-10-819 TT 113 genotypes are associated with reduced risk of gastric cancer in Asian populations, whereas the IL-10-1082 GG-plus-GA genotypes are associated with increased risk (especially intestinal-type gastric cancer) in Asian populations. 114 Though many genetic polymorphisms have been linked to altered gastric cancer susceptibility, no genetic tests exist in clinical practice.…”

Section: Discovery Of Novel Biomarkersmentioning

confidence: 99%