Ontology highlight
ABSTRACT:
PROVIDER: PRJNA685500 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13264300_1.fastq.gz | Fastqsanger.gz | |||
| SRR13264300_2.fastq.gz | Fastqsanger.gz | |||
| SRR13264301_1.fastq.gz | Fastqsanger.gz | |||
| SRR13264301_2.fastq.gz | Fastqsanger.gz | |||
| SRR13264302_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 318 |
Similar Datasets
Project description:Chronic infection with the bacterial pathogen Helicobacter pylori is a risk factor for the development of gastric cancer, yet remains asymptomatic in a majority of individuals. We report here that the C57Bl6 mouse model of experimental infection with the closely related H. felis recapitulates this wide range in host susceptibility. A majority of infected mice develop premalignant lesions such as gastric atrophy, compensatory epithelial hyperplasia and intestinal metaplasia, whereas a minority is completely protected from preneoplasia. Protection is associated with the failure to mount an IFN-gamma response to the infection and an associated high Helicobacter burden. We demonstrate that IFN-gamma is essential for clearance of Helicobacter, but also mediates the formation of preneoplastic lesions. We further provide evidence that IFN-gamma triggers a specific transcriptional program in murine gastric epithelial cells in vitro and in vivo, and induces their preferential transformation to the hyperplastic phenotype. In summary, our data suggest a dual role for IFN-gamma in Helicobacter pathogenesis that could provide an explanation for the differential susceptibility to H. pylori-induced gastric pathology in the human population. Keywords: response to in vitro stimulus / comparison of histopathological states We chose mice for gene expression profiling that following Helicobacter infection had (a) symptoms of gastritis, but no epithelial changes, (b) atrophic gastritis accompanied by corpus gland hyperplasia or (c) atrophic gastritis accompanied by intestinal metaplasia. An uninfected control group was also included in the analysis, as were two groups of mice that lacked mature T- and B-cells due to a deletion mutation in the rag1 gene (Rag-1-/-) and that were either experimentally infected or served as Rag-1-/- uninfected controls. To see the effects of IFNg on murine gastric epithelial cells we analysed an immortalized murine primary gastric epithelial cell line treated with three different concentrations of IFNg in comparison to an untreated control.
2009-03-05 | E-GEOD-13873 | biostudies-arrayexpress
Project description:Chronic infection with the bacterial pathogen Helicobacter pylori is a risk factor for the development of gastric cancer, yet remains asymptomatic in a majority of individuals. We report here that the C57Bl6 mouse model of experimental infection with the closely related H. felis recapitulates this wide range in host susceptibility. A majority of infected mice develop premalignant lesions such as gastric atrophy, compensatory epithelial hyperplasia and intestinal metaplasia, whereas a minority is completely protected from preneoplasia. Protection is associated with the failure to mount an IFN-gamma response to the infection and an associated high Helicobacter burden. We demonstrate that IFN-gamma is essential for clearance of Helicobacter, but also mediates the formation of preneoplastic lesions. We further provide evidence that IFN-gamma triggers a specific transcriptional program in murine gastric epithelial cells in vitro and in vivo, and induces their preferential transformation to the hyperplastic phenotype. In summary, our data suggest a dual role for IFN-gamma in Helicobacter pathogenesis that could provide an explanation for the differential susceptibility to H. pylori-induced gastric pathology in the human population. Keywords: response to in vitro stimulus / comparison of histopathological states
2009-03-05 | GSE13873 | 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: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:We have previously reported human gastrin overexpressing transgenic mice (=INS-GAS mice) and Helicobacter felis (=H.felis) infection synergistically accelerated gastric cancer in mice stomachs. (Wang et al 2000) Using this mouse model, we employed microarray analysis of gene expression profiling to identify gastric cancer-specific genes. Keywords: disease state analysis
2006-04-13 | GSE4651 | 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. human Samples: Human gastric tumor cell line, N87 was grown in RPMI1640 supplemented with 10% fetal bovine serum. ChIP assays were performed using anti-FOXD3 antibody. The immunoprecipitated-FOXD3 and -IgG DNA were used to probe the Agilent human ChIP-chip arrays. mouse Samples: Two-condition experiment, H pylori-infected vs. control gastric tissues. 2 dye-swap replicates.
2012-12-28 | E-GEOD-39490 | biostudies-arrayexpress
Project description:Background: Helicobacter pylori (H. pylori) infection is a known cause of many digestive diseases, including gastritis, peptic ulcers, and gastric cancer. However, the underlying mechanism(s)by which H. pylori infection triggers these disorders are still not clearly understood. Methods: We have developed an accelerated disease progression mouse model, which leverages mice deficient in the myeloid differentiation primary response 88 gene (Myd88-/-) infected with Helicobacter felis (H. felis) Findings: In this study, we found that H. felis-induced inflammation in Myd88-/- mice progressed to high-grade dysplasia, driven by activation of the type I interferon (IFN-I) signaling pathway and upregulation of its downstream targets, IFN-stimulated genes (ISGs). We also observed enrichment of IFN stimulated-response element (ISRE) motifs in the promoters of upregulated genes, further supporting the involvement of this pathway. In contrast, mice deficient in Toll/interleukin-1 receptor (TIR)-domain-containing adaptor inducing interferon-β (TRIF, TrifLps2) did not progress to severe gastric pathology after H. felis infection, implicating the TRIF signaling pathway in disease pathogenesis and progression. Additionally, analysis of gastric biopsy samples from human gastric cancer patients illustrated that low expression of Myd88 and high expression of Trif were both significantly correlated with poor survival. Interpretation: Our study using an accelerated animal model for gastric cancer and gastric biopsy samples from patients demonstrated that activation of the TRIF-IFN-I signaling pathway promotes Helicobacter-induced disease progression toward severe gastric pathology and gastric cancer development. This represents a potential target for therapeutic intervention, and further exploration may lead to the identification of novel treatment strategies.
2024-04-17 | GSE250438 | GEO
Project description:Helicobacter pylori infection can induce gastric pathologies ranging from chronic gastritis to peptic ulcers and gastric cancer. Individuals´ response to H. pylori infection is complex and it depends on a combination of environmental factors, genetic background, host response and strain virulence. The pathway towards gastric cancer is a sequence of events known as the Correa's model of gastric carcinogenesis, a stepwise inflammatory process from normal mucosa to chronic active gastritis, atrophy, metaplasia and finally gastric adenocarcinoma. This study explores gastric clinical specimens representing different steps of the Correa pathway with the aim of identifying the expression profile of coding- and non-coding RNAs (microRNAs and small RNAs) which may have a role in the Correa's model of gastric carcinogenesis and potentially develop novel clinical biomarkers. We screened for differentially expressed genes in gastric biopsies (antrum/corpus) by employing RNAseq (for microRNAs and non-coding RNAs) and microarrays (for coding RNAs).
2020-09-01 | E-MTAB-8889 | biostudies-arrayexpress
Project description:Helicobacter pylori infection can induce gastric pathologies ranging from chronic gastritis to peptic ulcers and gastric cancer. Individuals´ response to H. pylori infection is complex and it depends on a combination of environmental factors, genetic background, host response and strain virulence. The pathway towards gastric cancer is a sequence of events known as the Correa's model of gastric carcinogenesis, a stepwise inflammatory process from normal mucosa to chronic active gastritis, atrophy, metaplasia and finally gastric adenocarcinoma. This study explores gastric clinical specimens representing different steps of the Correa pathway with the aim of identifying the expression profile of coding- and non-coding RNAs (microRNAs and small RNAs) which may have a role in the Correa's model of gastric carcinogenesis and potentially develop novel clinical biomarkers. We screened for differentially expressed genes in gastric biopsies (antrum/corpus) by employing RNAseq (for microRNAs and non-coding RNAs) and microarrays (for coding RNAs).
2020-09-01 | E-MTAB-8890 | biostudies-arrayexpress
Project description:Helicobacter pylori infection can induce gastric pathologies ranging from chronic gastritis to peptic ulcers and gastric cancer. Individuals´ response to H. pylori infection is complex and it depends on a combination of environmental factors, genetic background, host response and strain virulence. The pathway towards gastric cancer is a sequence of events known as the Correa's model of gastric carcinogenesis, a stepwise inflammatory process from normal mucosa to chronic active gastritis, atrophy, metaplasia and finally gastric adenocarcinoma. This study explores gastric clinical specimens representing different steps of the Correa pathway with the aim of identifying the expression profile of coding- and non-coding RNAs (microRNAs and small RNAs) which may have a role in the Correa's model of gastric carcinogenesis and potentially develop novel clinical biomarkers. We screened for differentially expressed genes in gastric biopsies (antrum/corpus) by employing RNAseq (for microRNAs and non-coding RNAs) and microarrays (for coding RNAs).
2020-09-01 | E-MTAB-8896 | biostudies-arrayexpress