DNA methylation profiles in gastric mucosa samples with low, intermediate and high cancer risk
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE226818 | GEO | 2024/03/31
REPOSITORIES: GEO
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Project description:The whole-genome oligonucleotide microarray analysis gives an opportunity for studying the unidentified gene expression background of the idiopathic and H.pylori related gastric erosive alterations. Using microarrays we compared the whole genome gene expression profile of HP+ and HP- gastric erosions and normal adjacent mucosa to explain the possible role and response to HP infection and to get morphology related mRNA expression patterns. Experiment Overall Design: Total RNA was extracted from frozen gastric biopsy specimens of patients with Helicobacter pylori positive (HP+) and Helicobacter pylori negative (HP-) antrum erosions (ER+), and the corresponding, adjacent normal mucosae (ER-) and hybridized on Affymetrix HGU133 Plus 2.0 microarrays
2008-06-18 | E-GEOD-5081 | biostudies-arrayexpress
Project description:We performed the expression RNA-seq experiments for mRNA of gastric cancer tissue. Most of gastric cancers (GCs) are accompanied by Helicobacter pylori (HP) infection. However, a very limited fraction lacks any signs of HP infection and exhibits early-stage diffuse (ED) phenotype. Although previous genomic cohorts have identified multiple driver mutations for gastric cancers including diffuse-type histology, any driver event of GC without HP has not been elucidated. The present study aims to explore the molecular mechanism with comprehensive genomic and transcriptomic analyses by comparing EDGC with and without HP. EDGCs were classified as HP-negative based on the following criteria: 1) no antibiotic eradication history, 2) no atrophic appearance by endoscopy, 3) no atrophic appearance by histology, 4) negativity in two or more tests such as rapid urease, urease breath, serum antibody, stool antigen and serum pepsinogen tests. DNAs and RNAs were extracted from EDGCs with over 10 mm in diameter to secure sufficient amount of cancer tissues. Laser-capture microdissection was then used to reduce contamination of normal cells for further molecular assays. For transcriptome analyses, we conducted RNA-seq of 2 HP-positive and 4 HP-negative fresh frozen EDGCs obtained endoscopically
2022-03-25 | GSE129219 | GEO
Project description:Persistent colonization of the gastric mucosa by Helicobacter pylori (Hp) elicits chronic inflammation and aberrant epithelial cell proliferation, which increases the risk of gastric cancer. We examined the ability of microRNAs to modulate gastric cell proliferation in response to persistent Hp infection and found that epigenetic silencing of miR-210 plays a key role in gastric disease progression. Importantly, DNA methylation of the miR-210 gene was increased in Hp-positive human gastric biopsies as compared to Hp-negative controls. Moreover silencing of miR-210 in gastric epithelial cells promoted proliferation. We identified STMN1 and DIMT1 as miR-210 target genes and demonstrated that inhibition of miR-210 expression augmented cell proliferation by activating STMN1 and DIMT1. Together, our results highlight inflammation-induced epigenetic silencing of miR-210 as a mechanism of induction of chronic gastric diseases, including cancer, during Hp infection.
2014-09-04 | GSE58004 | GEO
Project description:Even after endoscopic treatment of early gastric adenocarcinoma (GAC) and eradication of Helicobacter pylori (H. pylori), some patients develop a metachronous recurrence (MR), the mechanism of which is still unknown. To elucidate the mechanism and risk factors for MR, we analyzed gene expression at multiple locations of the gastric mucosa, considering the heterogeneity of gastric mucosal damage caused by H. pylori infection and investigated the mechanism and risk factors for MR.
2022-12-31 | GSE190455 | GEO
Project description:Even after endoscopic treatment of early gastric adenocarcinoma (GAC) and eradication of Helicobacter pylori (H. pylori), some patients develop a metachronous recurrence (MR), the mechanism of which is still unknown. To elucidate the mechanism and risk factors for MR, we analyzed gene expression at multiple locations of the gastric mucosa, considering the heterogeneity of gastric mucosal damage caused by H. pylori infection and investigated the mechanism and risk factors for MR.
2022-12-31 | GSE190449 | GEO
Project description:Persistent colonization of the gastric mucosa by Helicobacter pylori (Hp) elicits chronic inflammation and aberrant epithelial cell proliferation, which increases the risk of gastric cancer. We examined the ability of microRNAs to modulate gastric cell proliferation in response to persistent Hp infection and found that epigenetic silencing of miR-210 plays a key role in gastric disease progression. Importantly, DNA methylation of the miR-210 gene was increased in Hp-positive human gastric biopsies as compared to Hp-negative controls. Moreover silencing of miR-210 in gastric epithelial cells promoted proliferation. We identified STMN1 and DIMT1 as miR-210 target genes and demonstrated that inhibition of miR-210 expression augmented cell proliferation by activating STMN1 and DIMT1. Together, our results highlight inflammation-induced epigenetic silencing of miR-210 as a mechanism of induction of chronic gastric diseases, including cancer, during Hp infection. To identify miR-210 targets in gastric cells, whole transcriptome analysis of AGS and MKN45 cells transfected with pre-miR-210 was conducted using Affymetrix GeneChip Human Genome U133 Plus 2.0 Array.
2014-09-04 | E-GEOD-58004 | biostudies-arrayexpress
Project description:Interventions: Drug : 1.At the time of EMR/ESD: Rapid Urease test/anti-helicobacter IgG Ab/ histology --> If two of them are (+), diagnosis of HP infection could be made. During endoscopy, designated biopsy for the evaluation of gastric atrophy should be performed (baseline data)
2.Patients are assigned to HP (+) or HP (-) group according to the HP status. (Each 120 patients)
3.HP (+) group should undergo eradication therapy after anti-ulcer medication (8weeks, LFDT 30mg + rebamipide SR 150mg bid), and diagnosis of successful eradication should be followed with urea breath test 4weeks later of last dose.
4.HP (-) group should undergo anti-ulcer medication (8weeks, LFDT 30mg + rebamipide SR 150mg bid).
5.In this time, patients are randomly allocated to rebamipide group (60 patients from each group) or placebo group (60 patients from each group).
EGD with biopsy should be repeated to evaluate the regression of atrophy at the time of 12mo, 24mo, 36mo, 48mo, 60mo, respectively.
Primary outcome(s): The primary outcome of this study is to evaluate the difference in the effect of between rebamipide and placebo on regression of gastric atrophy and intestinal metaplasia.
Primary Purpose : Treatment, Intervention Model : Parallel, Blinding/Masking : , Blinding Target : Subject, Investigator, Caregiver, Allocation : RCT
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Project description:Carcinogenic bacteria, Helicobacter pylori, induce DNA double-strand breaks in infected host cells. Therefore, we have investigated which genes are upregulated after the infection. Although Helicobacter pylori infection is etiologically related to the inflammation-related malignancy, gastric cancers, it role in the molecular pathogenesis of disease remains unclear. In vitro studies have suggested the infection may cause breaks in double-stranded DNA. We used microarray analysis of H. pylori-infected human gastric biopsies to investigate the effect of H. pylori on gene expression genes involved in DNA repair and DNA damage response. Micro-array analysis and immunohistochemistory showed that ATM (ataxia-telangiectasia mutated) was upregulated in H. pylori gastritis but down regulated in the premalignant lesion, intestinal metaplasia. Studies in gastric cancer cell lines showed that H. pylori-infection induced activation of ATM and formation of ?-H2AX. ?-H2AX formation was present following infection with bout cag pathogenicity island (PAI)- positive and negative strains but more robust with cag PAI positive strains consistent with the fact that both cag PAI positive negative strains are associated with gastric cancer but the risk is higher with cag PAI positive strains. Eradication of H. pylori infection is associated with a reduction in cancer risk even in the most high risk populations. These data provide a plausible molecular mechanism for a direct bacterial-host interaction increasing cancer risk. To identify tumor suppressors affected by H. pylori-infection, microarray screening was used to compare the gene expression profiles of AGS cells, a gastric cancer cell line, infected with various mutants of H. pylori.
2014-08-23 | E-GEOD-60661 | biostudies-arrayexpress
Project description:Carcinogenic bacteria, Helicobacter pylori, induce DNA double-strand breaks in infected host cells, while ATM-dependent DNA damage responses in host cells suppress genome instabilities caused by DNA breakages, which resulting in the suppression of H. pylori-induced gastric cancers. Although Helicobacter pylori infection is etiologically related to the inflammation-related malignancy, gastric cancers, it role in the molecular pathogenesis of disease remains unclear. In vitro studies have suggested the infection may cause breaks in double-stranded DNA. We used microarray analysis of H. pylori-infected human gastric biopsies to investigate the effect of H. pylori on gene expression genes involved in DNA repair and DNA damage response. Micro-array analysis and immunohistochemistory showed that ATM (ataxia-telangiectasia mutated) was upregulated in H. pylori gastritis but down regulated in the premalignant lesion, intestinal metaplasia. Studies in gastric cancer cell lines showed that H. pylori-infection induced activation of ATM and formation of γ-H2AX. γ-H2AX formation was present following infection with bout cag pathogenicity island (PAI)- positive and negative strains but more robust with cag PAI positive strains consistent with the fact that both cag PAI positive negative strains are associated with gastric cancer but the risk is higher with cag PAI positive strains. Eradication of H. pylori infection is associated with a reduction in cancer risk even in the most high risk populations. These data provide a plausible molecular mechanism for a direct bacterial-host interaction increasing cancer risk. To identify tumor suppressors affected by H. pylori-infection, microarray screening was used to compare the gene expression profiles of gastric mucosa obtained from individuals with H. pylori-gastritis and with intestinal metaplasia with tissue from uninfected controls.
2014-08-18 | E-GEOD-47797 | biostudies-arrayexpress
Project description:Carcinogenic bacteria, Helicobacter pylori, induce DNA double-strand breaks in infected host cells, while ATM-dependent DNA damage responses in host cells suppress genome instabilities caused by DNA breakages, which resulting in the suppression of H. pylori-induced gastric cancers. Although Helicobacter pylori infection is etiologically related to the inflammation-related malignancy, gastric cancers, it role in the molecular pathogenesis of disease remains unclear. In vitro studies have suggested the infection may cause breaks in double-stranded DNA. We used microarray analysis of H. pylori-infected human gastric biopsies to investigate the effect of H. pylori on gene expression genes involved in DNA repair and DNA damage response. Micro-array analysis and immunohistochemistory showed that ATM (ataxia-telangiectasia mutated) was upregulated in H. pylori gastritis but down regulated in the premalignant lesion, intestinal metaplasia. Studies in gastric cancer cell lines showed that H. pylori-infection induced activation of ATM and formation of γ-H2AX. γ-H2AX formation was present following infection with bout cag pathogenicity island (PAI)- positive and negative strains but more robust with cag PAI positive strains consistent with the fact that both cag PAI positive negative strains are associated with gastric cancer but the risk is higher with cag PAI positive strains. Eradication of H. pylori infection is associated with a reduction in cancer risk even in the most high risk populations. These data provide a plausible molecular mechanism for a direct bacterial-host interaction increasing cancer risk. To identify tumor suppressors affected by H. pylori-infection, microarray screening was used to compare the gene expression profiles of gastric mucosa obtained from individuals with H. pylori-gastritis and with intestinal metaplasia with tissue from uninfected controls.
2014-08-23 | E-GEOD-60662 | biostudies-arrayexpress