scholarly journals DNA Methylation Silencing of microRNA Gene Methylater in the Precancerous Background Mucosa with and without Gastric Cancer: Analysis of Effects of Helicobacter pylori Eradication and Long-Term Aspirin Use

2019 ◽  
Author(s):  
Jiro Watari ◽  
Chiyomi Ito ◽  
Tadakazu Shimoda ◽  
Toshihiko Tomita ◽  
Tadayuki Oshima ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Dna Methylation ◽  
Helicobacter Pylori ◽  
Early Stage ◽  
Surrogate Marker ◽  
Predictive Marker ◽  
Microrna Gene ◽  
H Pylori ◽  
Background Mucosa

The risk of gastric cancer (GC) declines after Helicobacter pylori (H. pylori) eradication and long-term aspirin use. We evaluated the effects of H. pylori eradication (Cohort 1) and aspirin use (Cohort 2) on the methylation of microRNAs (miRNAs) such as miR-34c, miR-124a-3, miR-129-2, and miR-137 in the gastric mucosa with and without GC, i.e., atrophic mucosa (AM) and intestinal metaplasia (IM). DNA was isolated from AM and IM separately using laser caption microdissection. In Cohort 1, H. pylori eradication was associated with a significant reduction of miR-124a-3 methylation only in AM, but not in IM. miR-129-2 methylation in AM may be a surrogate marker of GC in H. pylori-infected patients. In Cohort 2, aspirin did not reverse miRNA methylation in either AM or IM irrespective of H. pylori infection. miR-129-2 methylation in AM was an independent predictive marker of GC in H. pylori-infected but not -eradicated patients. These results indicate that H. pylori eradication and aspirin use were less effective in improving methylation in IM compared with AM; thus, these interventions are recommended at an early stage prior to the development of IM to prevent GC development.

scholarly journals Long-term Changes In Aberrant DNA Methylation And Gastritis After Helicobacter Pylori Eradication Focused On Metachronous Gastric Cancer

2021 ◽  
Author(s):  
Ikko Tanaka ◽  
Shoko Ono ◽  
Yoshiyuki Watanabe ◽  
Hiroyuki Yamamoto ◽  
Ritsuko Oikawa ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Dna Methylation ◽  
Helicobacter Pylori ◽  
Methylation Level ◽  
Aberrant Methylation ◽  
Long Term Changes ◽  
Metachronous Gastric Cancer ◽  
Aberrant Dna Methylation ◽  
H Pylori

Abstract BackgroundA persistently high methylation level in gastric mucosa after Helicobacter pylori (H. pylori) eradication is presumed to be a risk for metachronous gastric cancer (MGC); however, long-term changes in aberrant DNA methylation and histological gastritis have been unclear. Our aim was to examine changes in DNA methylation and histological gastritis according to the occurrence of MGC.MethodsSubjects were classified into 3 groups: 25 patients in whom metachronous gastric cancers occurred after the initial endoscopic resection (ER) for early gastric cancer and H. pylori eradication (MGC group), 17 patients in whom MGC did not occur for more than 5 years after initial ER and H. pylori eradication (non-MGC group) and 29 patients without a history of gastric cancer who succeeded in eradication more than 5 years ago (HP group). Aberrance of DNA methylation in 3 genes (miR-124a-3, EMX1, NKX6-1) and histological score of atrophy and intestinal metaplasia (IM) were evaluated using biopsy samples before and more than a mean of 5 years after H. pylori eradication.ResultsThe methylation level of miR-124a-3 in the HP group and non-MGC group and that of EMX1 in the HP group significantly decreased in the long term after eradication. In the MGC group, H. pylori eradication did not improve aberrant methylation, and the Z-score significantly increased. There were significant positive correlations between methylation levels in miR-124a-3 and EMX1 and histological findings after eradication.ConclusionsA persistently high methylation level after H. pylori eradication reflected precancerous mucosal conditions and led to long-term MGC.

Prevalence of Helicobacter pylori infection among blood donors in Saxony-Anhalt, Germany – a region at intermediate risk for gastric cancer

2017 ◽  
Vol 55 (07) ◽  
pp. 653-656 ◽  
Author(s):  
Caspar Franck ◽  
Armin Hoffmann ◽  
Alexander Link ◽  
Christian Schulz ◽  
Kerstin Wuttig ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Blood Donors ◽  
Eradication Therapy ◽  
Surrogate Marker ◽  
University Hospital ◽  
Study Cohort ◽  
Emergency Ward ◽  
Age Related ◽  
H Pylori

Abstract Background In the federal state of Saxony-Anhalt, gastric cancer (GC) incidence ranks among the highest in Germany. Helicobacter pylori prevalence is a surrogate marker for GC risk in a given population. In 2010 we reported an H. pylori seroprevalence of 44.4 % in patients at the emergency ward of the University Hospital of Magdeburg, the capital of Saxony-Anhalt. Our aim is to update these findings in a cohort of healthy blood donors from the same region. Materials and methods The sera of 516 consecutive blood donors (40.1 ± 14.1 years; 286 males and 230 females) were tested for antibodies against H. pylori and CagA. Data on demographics and previous H. pylori eradication therapy were obtained by means of a structured questionnaire. Blood donors with positive serology for H. pylori or CagA and/or history of eradication therapy were classified as H. pylori-positive. Results Overall, 28.9 % of the study cohort were H. pylori-positive. The prevalence was higher in older generations (9 % in 18 – 20 years up to 47 % in 61 – 70 years). In 44.4 % of H. pylori IgG-positive donors, CagA serology was also positive. This proportion was not age-dependent. Study participants with siblings were by trend more often H. pylori-positive (p = 0.066). Conclusion Compared to our previous study in patients at the emergency ward, we found by trend lower age-related H. pylori prevalence rates. In our cohort of healthy blood donors, we confirmed a lower H. pylori prevalence in younger generations.

scholarly journals Discovery and Validation of Novel Methylation Markers in Helicobacter pylori-Associated Gastric Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Huan Wang ◽  
Nian-Shuang Li ◽  
Cong He ◽  
Chuan Xie ◽  
Yin Zhu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Dna Methylation ◽  
Helicobacter Pylori ◽  
Gene Expression Data ◽  
Functional Enrichment ◽  
Expression Data ◽  
H Pylori

Previous studies have shown that abnormal methylation is an early key event in the pathogenesis of most human cancers, contributing to the development of tumors. However, little attention has been given to the potential of DNA methylation patterns as markers for Helicobacter pylori- (H. pylori-) associated gastric cancer (GC). In this study, an integrated analysis of DNA methylation and gene expression was conducted to identify some potential key epigenetic markers in H. pylori-associated GC. DNA methylation data of 28 H. pylori-positive and 168 H. pylori-negative GC samples were compared and analyzed. We also analyzed the gene expression data of 18 H. pylori-positive and 145 H. pylori-negative GC cases. Finally, the results were verified by in vitro and in vivo experiments. A total of 5609 differentially methylated regions associated with 2454 differentially methylated genes were identified. A total of 228 differentially expressed genes were identified from the gene expression data of H. pylori-positive and H. pylori-negative GC cases. The screened genes were analyzed for functional enrichment. Subsequently, we obtained 28 genes regulated by methylation through a Venn diagram, and we identified five genes (GSTO2, HUS1, INTS1, TMEM184A, and TMEM190) downregulated by hypermethylation. HUS1, GSTO2, and TMEM190 were expressed at lower levels in GC than in adjacent samples ( P < 0.05 ). Moreover, H. pylori infection decreased HUS1, GSTO2, and TMEM190 expression in vitro and in vivo. Our study identified HUS1, GSTO2, and TMEM190 as novel methylation markers for H. pylori-associated GC.

scholarly journals Gastric xanthelasma: case report

2020 ◽  
Vol 7 (2) ◽  
pp. 594
Author(s):  
Ana C. Almeida ◽  
Emília C. Fraga ◽  
Cristina P. Camacho ◽  
Maria J. Amaral ◽  
António Milheiro ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Case Report ◽  
Predictive Marker ◽  
Gastric Antrum ◽  
Complete Regression ◽  
Upper Gi ◽  
H Pylori ◽  
Single Lesion ◽  
Development Of Gastric Cancer

Xanthelasma, also known as Xanthoma or lipid island, is an uncommon gastrointestinal tract (GIT) tumor-like lesion and the stomach is its most frequent location in upper GI lesions, specifically in the gastric antrum, as a single lesion. The pathogenesis appears to be related to healing processes in response to tissue damage provoked by inflammation induced by Helicobacter pylori infection. Many studies have reported that successful H. pylori eradication helps prevent gastric cancer (GC) development. We present a case of a 77 years old patient that showed endoscopic diagnosis of erythematous gastropathy, a gastric antrum xanthelasma and H. Pylori infection. After confirmed H. pylori eradication, the lesion had complete regression. The successful eradication of H. pylori probably led to a total regression of the lesion. Gastric xanthelasma (GX) has been shown to be an independent predictive marker for early GC detection after H. pylori eradication. GX could be a useful marker for predicting the development of gastric cancer.

scholarly journals Mass eradication of Helicobacter pylori to reduce gastric cancer incidence and mortality: a long-term cohort study on Matsu Islands

Gut ◽  
2020 ◽  
pp. gutjnl-2020-322200 ◽  
Author(s):  
Tsung-Hsien Chiang ◽  
Wei-Jung Chang ◽  
Sam Li-Sheng Chen ◽  
Amy Ming-Fang Yen ◽  
Jean Ching-Yuan Fann ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Cancer Incidence ◽  
Control Period ◽  
Eradication Therapy ◽  
Incidence Rates ◽  
Long Term Effects ◽  
Incidence And Mortality ◽  
H Pylori

ObjectiveAlthough mass eradication of Helicobacter pylori has been proposed as a means to eliminate gastric cancer, its long-term effects remain unclear.DesignMass eradication of H. pylori infection was launched in 2004 and continued until 2018 for a high-risk Taiwanese population aged 30 years or older dwelling on Matsu Islands with prevalent H. pylori infection. Test positives for the 13C-urea breath test underwent eradication therapy. We evaluated the effectiveness of the mass eradication in reducing two main outcomes, incidence and mortality rates of gastric cancer, until the end of 2016 and 2018, respectively.ResultsAfter six rounds of mass screening and eradication, the coverage rate reached 85.5% (6512/7616). The referral rate for treatment was 93.5% (4286/4584). The prevalence rates of H. pylori fell from 64.2% to 15.0% with reinfection rates of less than 1% per person-year. The presence and severity of atrophic gastritis and intestinal metaplasia also decreased with time. Compared with the historical control period from 1995 to 2003, the effectiveness in reducing gastric cancer incidence and mortality during the chemoprevention period was 53% (95% CI 30% to 69%, p<0.001) and 25% (95% CI −14% to 51%, p=0.18), respectively. No significant changes were noted in the incidence rates of other digestive tract cancers or the antibiotic resistance rate of H. pylori.ConclusionPopulation-based eradication of H. pylori has significantly reduced gastric cancer incidence with no increase in the likelihood of adverse consequences. A significant reduction in mortality is likely to be achieved with a longer follow-up period.Trial registration numberNCT00155389

scholarly journals Helicobacter pylori-induced DNA Methylation as an Epigenetic Modulator of Gastric Cancer: Recent Outcomes and Future Direction

Pathogens ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 23 ◽  
Author(s):  
Jibran Muhammad ◽  
Mohamed Eladl ◽  
Ghalia Khoder
Keyword(s):  
Gastric Cancer ◽  
Dna Methylation ◽  
Helicobacter Pylori ◽  
Epigenetic Drugs ◽  
Mesh Terms ◽  
Potential Benefits ◽  
H Pylori ◽  
Future Direction ◽  
Methylating Agents

Gastric cancer is ranked fifth in cancer list and has the third highest mortality rate. Helicobacter pylori is a class I carcinogen and a predominant etiological factor of gastric cancer. H. pylori infection may induce carcinogenesis via epigenetic alterations in the promoter region of various genes. H. pylori is known to induce hypermethylation-silencing of several tumor suppressor genes in H. pylori-infected cancerous and H. pylori-infected non-cancerous gastric mucosae. This article presents a review of the published literature mainly from the last year 15 years. The topic focuses on H. pylori-induced DNA methylation linked to gastric cancer development. The authors have used MeSH terms “Helicobacter pylori” with “epigenetic,” “DNA methylation,” in combination with “gastric inflammation”, gastritis” and “gastric cancer” to search SCOPUS, PubMed, Ovid, and Web of Science databases. The success of epigenetic drugs such as de-methylating agents in the treatment of certain cancers has led towards new prospects that similar approaches could also be applied against gastric cancer. However, it is very important to understand the role of all the genes that have already been linked to H. pylori-induced DNA methylation in order to in order to evaluate the potential benefits of epigenetic drugs.

scholarly journals Long-term persistence of gastric dysbiosis after eradication of Helicobacter pylori in patients who underwent endoscopic submucosal dissection for early gastric cancer

2020 ◽  
Author(s):  
Toshio Watanabe ◽  
Yuji Nadatani ◽  
Wataru Suda ◽  
Akira Higashimori ◽  
Koji Otani ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Endoscopic Submucosal Dissection ◽  
Eradication Therapy ◽  
Bacterial Composition ◽  
Submucosal Dissection ◽  
History Of ◽  
H Pylori

Abstract Background Gastric microbiome, other than Helicobacter pylori, plays a role in the tumorigenesis of gastric cancer (GC). Patients who undergo endoscopic submucosal dissection for early GC have a high risk of developing metachronous GC even after successful eradication of H. pylori. Thus, we investigated the microbial profiles and associated changes in such patients after the eradication of H. pylori. Methods A total of 19 H. pylori-infected patients with early GC who were or to be treated by endoscopic resection, with paired biopsy samples at pre- and post-eradication therapy, were retrospectively enrolled. Ten H. pylori-negative patients were enrolled as controls. Biopsy samples were analyzed using 16S rRNA sequencing. Results H. pylori-positive patients exhibited low richness and evenness of bacteria with the deletion of several genera, including Blautia, Ralstonia, Faecalibacterium, Methylobacterium, and Megamonas. H. pylori eradication partially restored microbial diversity, as assessed during a median follow-up at 13 months after eradication therapy. However, post-eradication patients had less diversity than that in the controls and possessed a lower abundance of the five genera mentioned above. The eradication of H. pylori also altered the bacterial composition, but not to the same extent as that in controls. The microbial communities could be clustered into three separate groups: H. pylori-negative, pre-eradication, and post-eradication. Conclusion Changes in dysbiosis may persist long after the eradication of H. pylori in patients with a history of GC. Dysbiosis may be involved in the development of both primary and metachronous GC after the eradication of H. pylori in such patients.

scholarly journals Metachronous Gastric Cancer Occurring after Endoscopic Resection of Early Gastric Cancer

2020 ◽  
Vol 20 (4) ◽  
pp. 295-299
Author(s):  
Gwang Ha Kim
Keyword(s):  
Gastric Cancer ◽  
Endoscopic Resection ◽  
Early Stage ◽  
Long Term Outcomes ◽  
En Bloc ◽  
Gastric Cancers ◽  
Metachronous Gastric Cancer ◽  
H Pylori ◽  
Surveillance Endoscopy

Endoscopic resection (ER) has been widely used as a curative treatment for early gastric cancers (EGCs). Especially endoscopic submucosal dissection has several merits such as high en bloc and curative resection rates for EGCs and preservation of the entire stomach. However, ER has the inevitable limitation that the possibility of newly developing gastric cancers in the preserved stomach is still present. Metachronous gastric cancer (MGC) is defined as a newly developed gastric cancer occurring at a previously uninvolved site ≥1 year after the index ER of EGCs. The incidence of MGC is 3.3~15.6% and increases over time after ER. Old age, male sex, current smoking, severe atrophy and intestinal metaplasia, persistent Helicobacter pylori (H. pylori) infection, differentiated-type histology, and multiple initial gastric cancers are risk factors of MGC. As H. pylori eradication could reduce the risk of MGC after ER of EGCs, H. pylori eradication is strongly recommended for the prevention of MGC after ER of EGCs. Most MGCs are found at an early stage on regular surveillance endoscopy after ER and successfully treated with ER, with excellent long-term outcomes.

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