Helicobacter pylori
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA395900 | ENA |
REPOSITORIES: ENA
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Project description:Helicobacter pylori (H. pylori) is a human pathogen that infects almost half of the world’s population. Infection with H. pylori is frequently associated with chronic gastritis and can even lead to gastric and duodenal ulcers and gastric cancer. Although the persistent colonization of H. pylori and the development of H. pylori-associated gastritis remain poorly understood, it is believed that, in gastric mucosa, the modulated gastric epithelial cells (GECs) by H. pylori are key contributors. We used microarrays to detail the global programme of gene expression in Helicobacter pylori infected-gastric epithelial cell line AGS cells and identified up-regulated genes induced by Helicobacter pylori infection.
2024-04-18 | GSE264263 | GEO
Project description:Helicobacter pylori infection reprograms host gene expression and influences various cellular processes, which have been investigated by cDNA microarray in vitro culture cells and in vivo patients of the chronic abdominal complaint. In this study，the effects of H. pylori infection on host gene expression in the gastric antral mucosa of patients with chronic gastritis were examined.
2012-04-30 | GSE30042 | GEO
Project description:Helicobacter pylori infection reprograms host gene expression and influences various cellular processes, which have been investigated by cDNA microarray in vitro culture cells and in vivo patients of the chronic abdominal complaint. In this study，the effects of H. pylori infection on host gene expression in the gastric antral mucosa of patients with chronic gastritis were examined. The gastric antral mucosa was obtained from a total of 6 untreated patients undergoing gastroscopic and pathologic confirmation of chronic superficial gastritis. Three patients infected by H. pylori and 3 patients uninfected were used to cDNA microarray experiment.
2012-04-29 | E-GEOD-30042 | biostudies-arrayexpress
Project description:Helicobacter pylori clinical isolates can establish themselves in gastric epithelial stem cells and this interaction may have implications for gastric tumorigenesis. Mouse gastric epithelial progenitor cells (mGEPs) and non-progenitor gastric epithelial cells (npGECs) were infected for 24hrs with Helicobacter pylori clinical isolates Kx1 and Kx2. Kx1 was isolated from a patient with chronic atrophic gastritis (ChAG) and Kx2 from the same patient 4 years later, when he progressed to gastric adenocarcinoma. Keywords: RNA Expression Array
2008-02-22 | GSE10262 | GEO
Project description:Helicobacter pylori clinical isolates can establish themselves in gastric epithelial stem cells and this interaction may have implications for gastric tumorigenesis. Mouse gastric epithelial progenitor cells (mGEPs) were infected for 24hrs with Helicobacter pylori clinical isolates Kx1 and Kx2. Kx1 and Kx2 were also grown in cell media in the absence of cells. Kx1 was isolated from a patient with chronic atrophic gastritis (ChAG) and Kx2 from the same patient 4 years later, when he progressed to gastric adenocarcinoma. Keywords: RNA Expression Array
2008-02-22 | GSE10261 | GEO
Project description:Forkhead box (Fox) proteins constitute an evolutionarily conserved family of transcriptional regulators whose deregulations lead to tumorigenesis. However, their regulation and function in gastric cancer are unknown. Promoter hypermethylation occurs during Helicobacter pylori (H pylori)-induced gastritis, but whether the deregulated genes contribute to the multi-step gastric carcinogenesis remains unclear. FOXD3 was found to be hypermethylated in a mouse model of H pylori infection and possess tumor-suppressive functions in gastric cancer cell lines. In order to characterize the direct targets of FOXD3 that confer its actions, we performed ChIP-chip in N87 gastric cancer cell line which express low level of FOXD3 in the nuclei of a sub-population of cells. Promoter hypermethylation occurs during Helicobacter pylori (H pylori)-induced gastritis, but whether the deregulated genes contribute to the multi-step gastric carcinogenesis remains unclear. We used MethylCap-microarray to identify hypermethylated genes in a mouse model of H pylori infection.
2012-12-28 | GSE39490 | 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:Helicobacter pylori (H. pylori) infection is a key initiating factor in the Correa cascade of gastric carcinogenesis, but the comprehensive understanding of the pathogenic mechanisms underlying H. pylori-induced GC remains elusive. Here, we generated a single-cell atlas of gastric tumorigenesis comprising 18 specimens of gastritis, intestinal metaplasia and gastric cancer (GC) with or without H. pylori infection. We identified 48 distinct cell subpopulations including novel rare subtypes, and revealed the influence of H. pylori infection on cellular heterogeneity across neoplastic lesions.
2023-12-11 | GSE249874 | GEO
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.
2014-08-23 | GSE60662 | GEO
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