Global DNA hypomethylation is an early event in<i>Helicobacter pylori</i>-related gastric carcinogenesis

Compare, Debora; Rocco, Alba; Liguori, Eleonora; D’Armiento, Francesco Paolo; Persico, Giovanni; Masone, Stefania; Bottazzi, Enrico Coppola; Suriani, Renzo; Romano, Marco; Nardone, Gerardo

doi:10.1136/jcp.2010.087858

Cited by 51 publications

(50 citation statements)

References 32 publications

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“…Studies on H. pylori and Epstein-Barr virus infection have shown that the carcinogenic effect of both these pathogens is reinforced by inducing methylation changes in the gastric mucosa [72][73][74]. The methylation status in the tumor tissue resembles the patterns found in serum samples, so methylation status has the potential to become a noninvasive oncological marker exploitable in the early diagnosis of gastric cancer, and a novel target for cancer prevention [75].…”

Section: The Genetic Landscape Of Gastric Cancermentioning

confidence: 99%

Epidemiology of Gastric Cancer

2015

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Section: The Genetic Landscape Of Gastric Cancermentioning

confidence: 99%

Epidemiology of Gastric Cancer

2015

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“…These epigenetic changes correlate with the degree of gastric inflammation and increase with the development of premalignant changes of the gastric mucosa and finally gastric neoplasia [84,85,86]. Eradication of the infection can decrease general methylation levels [87], but this effect is not consistent for all affected genes [88].…”

Section: Host-related Factorsmentioning

confidence: 99%

“…The global methylation patterns which can also be assessed by a serum-based test can define different gastric cancer subtypes [93] and show a potential to be used as a marker to detect metastasis and therefore may reflect the malignant potential of gastric cancer [86,94]. …”

Section: Host-related Factorsmentioning

confidence: 99%

Helicobacter pylori and Gastric Cancer

Bornschein

Malfertheiner

2014

Dig Dis

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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.

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“…It was also observed that Hp infection increased microvillus formation and mucous secretion of the GES-1 gastric mucosa cells. In addition to local hypermethylation of CGIs, a global hypomethylationassessed by 5-methylcytosine immunostaining-was also described in Hp-positive chronic gastritis, independent of the CagA status (Compare et al 2011 ) . Analysis of repetitive elements by bisul fi te pyrosequencing showed hypomethylation of Alu and Sat-a repeats in Hp-infected gastric mucosae of healthy volunteers and GC patients, compared to Hp-negative control samples (Yoshida et al 2011 ) .…”

Section: Alterations Of the Host Cell Methylome In Helicobacter Pylormentioning

confidence: 93%