Working group report on schistosomes, liver flukes and <i>Helicobacter pylori</i>. Meeting held at IARC, LYON, 7–14 june 1994

Møller, Henrik; Heseltine, Élisabeth; Vainio, Harri

doi:10.1002/ijc.2910600502

Cited by 105 publications

(54 citation statements)

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“…Epidemiological studies in the last decade have established a strong causal relationship between Helicobacter pylori ( H. pylori ) infection and gastric cancer, and this bacteria has been classified as a Group I carcinogen by the World Health Organization (WHO) [1–3]. Previously, Correa suggested a human model of gastric carcinogenesis, and he postulated that the development of gastric cancer starts from chronic gastritis to gastric atrophy, intestinal metaplasia, dysplasia, and finally invasive cancer [4].…”

Section: Introductionmentioning

confidence: 99%

Association between Genetic Instability andHelicobacter pyloriInfection in Gastric Epithelial Dysplasia

Kim

Chung

Lee

et al. 2012

Gastroenterology Research and Practice

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Background. In gastric carcinogenesis, changes of DNA methylation appear to be an early molecular event, and the genome-wide methylation state is closely correlated with the level of long interspersed nucleotide element-1 (LINE-1) methylation. In this study, we measured LINE-1 methylation level according to genetic instability and evaluated the effect of Helicobacter pylori infection on genetic instability in gastric epithelial dysplasia. Methods. Total 100 tissue samples of gastric epithelial dysplasia were analyzed. Seven loci that linked to tumor suppressor genes were used to identify significant structural chromosomal aberrations. Microsatellite status was investigated for two different microsatellite marker loci (BAT25 and BAT26). Also, we measured LINE-1 methylation level by combined bisulfite restriction analysis (COBRA-LINE-1) method. Results. There were no significant differences of LINE-1 methylation level according to chromosomal/microsatellite instability and H. pylori state. In the dysplastic lesions with H. pylori infection, LINE-1 methylation level of MSI lesion was significantly lower than that of microsatellite stable (MSS) lesion (40.23 ± 4.47 versus 43.90 ± 4.81%, P < 0.01). Conclusions. In gastric epithelial dysplasia with H. pylori infection, MSI is correlated with reduced LINE-1 methylation level. Coexistence of H. pylori infection and MSI might be a driving force of gastric carcinogenesis.

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Section: Introductionmentioning

confidence: 99%

Association between Genetic Instability andHelicobacter pyloriInfection in Gastric Epithelial Dysplasia

Kim

Chung

Lee

et al. 2012

Gastroenterology Research and Practice

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“…Helicobacter pylori (Hp) has been implicated in the pathogenesis of most important gastroduodenal diseases, such as gastritis, peptic ulcer, gastric carcinoma and has been defined as a Class I carcinogen [1]. Hp can be subclassified into ‘cag’ pathogenicity island positive ( cag ) +ve and negative ( cag ) -ve strains based on the presence or absence of cag PAI, a 40-kb genome fragment containing 31 genes [2].…”

Section: Introductionmentioning

confidence: 99%

Curcumin Alleviates Matrix Metalloproteinase-3 and -9 Activities during Eradication of Helicobacter pylori Infection in Cultured Cells and Mice

Kundu

Pal

et al. 2011

PLoS ONE

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Current therapy-regimens against Helicobacter pylori (Hp) infections have considerable failure rates and adverse side effects that urge the quest for an effective alternative therapy. We have shown that curcumin is capable of eradicating Hp-infection in mice. Here we examine the mechanism by which curcumin protects Hp infection in cultured cells and mice. Since, MMP-3 and -9 are inflammatory molecules associated to the pathogenesis of Hp-infection, we investigated the role of curcumin on inflammatory MMPs as well as proinflammatory molecules. Curcumin dose dependently suppressed MMP-3 and -9 expression in Hp infected human gastric epithelial (AGS) cells. Consistently, Hp-eradication by curcumin-therapy involved significant downregulation of MMP-3 and -9 activities and expression in both cytotoxic associated gene (cag)+ve and cag -ve Hp-infected mouse gastric tissues. Moreover, we demonstrate that the conventional triple therapy (TT) alleviated MMP-3 and -9 activities less efficiently than curcumin and curcumin's action on MMPs was linked to decreased pro-inflammatory molecules and activator protein-1 activation in Hp-infected gastric tissues. Although both curcumin and TT were associated with MMP-3 and -9 downregulation during Hp-eradication, but unlike TT, curcumin enhanced peroxisome proliferator-activated receptor-γ and inhibitor of kappa B-α. These data indicate that curcumin-mediated healing of Hp-infection involves regulation of MMP-3 and -9 activities.

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“…Warren and Marshall first discovered Helicobacter pylori in 1982 1 . In the past two decades, the association of H. pylori and gastric cancers were well established 2–5 and H. pylori was classified as a group I carcinogen in 1994 6 . Eradication of H. pylori in gastric ulcer patients was associated with decreased risk of gastric cancer when compared with those with persistent infection 7 .…”

Section: Introductionmentioning

confidence: 99%

Prevalence and time trend of intestinal metaplasia in Hong Kong

Yee

Wong

Hui

et al. 2009

J of Gastro and Hepatol

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Working group report on schistosomes, liver flukes and Helicobacter pylori. Meeting held at IARC, LYON, 7–14 june 1994

Cited by 105 publications

References 1 publication

Association between Genetic Instability andHelicobacter pyloriInfection in Gastric Epithelial Dysplasia

Association between Genetic Instability andHelicobacter pyloriInfection in Gastric Epithelial Dysplasia

Curcumin Alleviates Matrix Metalloproteinase-3 and -9 Activities during Eradication of Helicobacter pylori Infection in Cultured Cells and Mice

Prevalence and time trend of intestinal metaplasia in Hong Kong

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