Altered mucosal DNA methylation in parallel with highly active Helicobacter pylori-related gastritis

Yoshida, Takeichi; Kato, Jun; Maekita, Takao; Yamashita, Satoshi; Enomoto, Shotaro; Ando, Takayuki; Niwa, Tohru; Deguchi, Hisanobu; Ueda, Kazuki; Inoue, Izumi; Iguchi, Mikitaka; Tamai, Hideyuki; Ushijima, Toshikazu; Ichinose, Masakazu

doi:10.1007/s10120-012-0230-x

Cited by 25 publications

(22 citation statements)

References 42 publications

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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%

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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Section: Host-related Factorsmentioning

confidence: 99%

Helicobacter pylori and Gastric Cancer

Bornschein

Malfertheiner

2014

Dig Dis

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“…Previous studies have also investigated the background tissues of numerous other malignancies (120)(121)(122). Yoshida et al (120) examined the methylation status of CpG islands in the promoter regions of six genes and two repetitive DNA elements in the gastric mucosae, and revealed that the methylation levels were consistently increased in a stepwise manner with activity of gastric inflammation, among patients who were H. pylori-negative, or had low-or high-titers (120), and concluded that evaluating DNA methylation levels in the gastric mucosae may predict the risk of gastric cancer.…”

Section: Studies Of Molecular Changes In Hcc Background Livermentioning

confidence: 99%

“…Yoshida et al (120) examined the methylation status of CpG islands in the promoter regions of six genes and two repetitive DNA elements in the gastric mucosae, and revealed that the methylation levels were consistently increased in a stepwise manner with activity of gastric inflammation, among patients who were H. pylori-negative, or had low-or high-titers (120), and concluded that evaluating DNA methylation levels in the gastric mucosae may predict the risk of gastric cancer. Lee et al (121) evaluated promoter region methylation of the cadherin 1 (CDH1) gene in the non-neoplastic mucosae of diffuse gastric cancer and revealed there was a significantly higher methylation ratio, compared with normal non-cancerous gastric mucosae.…”

Section: Studies Of Molecular Changes In Hcc Background Livermentioning

confidence: 99%

Molecular alterations in the carcinogenesis and progression of hepatocellular carcinoma: Tumor factors and background liver factors

et al. 2016

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Abstract. Although hepatocellular carcinoma (HCC) is associated with poor prognosis worldwide, the molecular mechanisms underlying the carcinogenesis and progression of this disease remain unclear. Several tumor characteristics have previously been demonstrated to be prognostic factors of survival following hepatic resection, or the recurrence of HCC or other types of cancer. Comparisons of normal tissues and HCC tumor tissues have revealed the presence of numerous molecular alterations in HCC, including genetic and epigenetic mechanisms, particularly mutations in certain genes and DNA methylation in the promoter regions of tumor-suppressor genes. A number of studies have previously used array analysis to detect variations in the expression levels of cancer-associated genes and microRNAs, and in DNA methylation. However, an investigation of HCC tumor tissues may not determine the effect of noncancerous liver tissues (background liver) in patients with HCC. As HCC may recur multicentrically following resection, a damaged or chronically diseased HCC background liver may be considered as a pre-cancerous organ. Therefore, the influence of the background liver on HCC requires further study. Detailed studies regarding the background liver may be essential for the improved understanding of the carcinogenesis and progression of this malignancy; however only a few studies have investigated the microenvironment of the HCC background liver. The present review discusses prior molecular studies of hepatocarcinogenesis that focus on HCC and background liver tissues.

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“…26,27 In non-cancerous inflammatory tissues, altered DNA methylation is evaluated as one of the early steps towards neoplastic change. 28 During the inflammation, the accumulation of DNA methylation contributes to the development of cancer. In noncancerous gastric mucosa, the presence of genes such as THBD, LOX, HRASLS, FLNc and HAND1 in methylated form, though rarely, supports the supposition that some gastric carcinogens are likely to induce methylation.…”

Section: H Pylori and Dna Methylation In Gcmentioning

confidence: 99%

The relationship between Helicobacter pylori and DNA hypermethylation in gastric cancer

Nursal

2015

Journal of Microbiology and Infectious Diseases

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Gastric cancer (GC) is one of the most common types of cancer across the world. GC carcinogenesis demonstrates a multi-step progression with the accumulation of genetic and epigenetic changes. The genetic changes on gene expression, without any change on deoxyribonucleic acid (DNA) sequencing, are named as "epigenetic". DNA methylation is the most commonly studied epigenetic modification in mammalians. Hypermethylation is observed on CpG (-Cphosphate-G-) islands In GC, promoter regions of genes. This is a significant mechanism that causes functional losses in tumor suppressor genes. In gastric cancer, DNA hypermethylation is seen in many genes. Helicobacter pylori (H. pylori) are a type of spiral-shaped Gram-negative bacteria. It infects approximately half of the world's population. H. pylori is an important etiological factor that causes GC in human beings. Chronic H. pylori infection in human is associated with hypermethylation of promoter sequences of different genes. This paper provides a review of the current literature on the relationship between H. pylori infection and DNA hypermethylation in GC. J Microbiol Infect Dis 2015;5(4): 187-190

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Altered mucosal DNA methylation in parallel with highly active Helicobacter pylori-related gastritis

Cited by 25 publications

References 42 publications

Helicobacter pylori and Gastric Cancer

Helicobacter pylori and Gastric Cancer

Molecular alterations in the carcinogenesis and progression of hepatocellular carcinoma: Tumor factors and background liver factors

The relationship between Helicobacter pylori and DNA hypermethylation in gastric cancer

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