Promoting research on opportunistic screening for gastric cancer based on colorectal cancer population screening
Ontology highlight
ABSTRACT:
DISEASE(S): Gastric Cancer Colorectal Cancer Combined Screening
PROVIDER: 88576 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:In this study, we treated the gastric cancer cell line AGS with PBS and Helicobacter pylori to perform RNA-seq analysis. A total of 18,308 different circRNA candidates were obtained in the experiment.Compared with the control, 101 significantly differentially expressed circRNAs were identified in the AGS cells infected with H. pylori, including 84 upregulated circRNAs and 17 downregulated circRNAs.Then, circMAN1A2 with the most significant expression difference was selected according to the sequencing results to study the epigenetic mechanism of H. pylori-induced gastric carcinogenesis.
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Project description:We are now trying to elucidate the mechanism of Helicobacter-induced gastritis and gastric cancer. To identify genes involved in these Helicobacter-associated diseases, we infected Helicobacter felis to INS-GAS (insulin-gastrin transgenic) mice (C57BL/6 background) which shows accelerated development of gastritis and gastric cancer.
2011-02-17 | GSE27361 | 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.
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Project description:Schilling2002 - Genome-scale metabolic
network of Helicobacter pylori (iCS291)
This model is described in the article:
Genome-scale metabolic model
of Helicobacter pylori 26695.
Schilling CH, Covert MW, Famili I,
Church GM, Edwards JS, Palsson BO.
J. Bacteriol. 2002 Aug; 184(16):
4582-4593
Abstract:
A genome-scale metabolic model of Helicobacter pylori 26695
was constructed from genome sequence annotation, biochemical,
and physiological data. This represents an in silico model
largely derived from genomic information for an organism for
which there is substantially less biochemical information
available relative to previously modeled organisms such as
Escherichia coli. The reconstructed metabolic network contains
388 enzymatic and transport reactions and accounts for 291 open
reading frames. Within the paradigm of constraint-based
modeling, extreme-pathway analysis and flux balance analysis
were used to explore the metabolic capabilities of the in
silico model. General network properties were analyzed and
compared to similar results previously generated for
Haemophilus influenzae. A minimal medium required by the model
to generate required biomass constituents was calculated,
indicating the requirement of eight amino acids, six of which
correspond to essential human amino acids. In addition a list
of potential substrates capable of fulfilling the bulk carbon
requirements of H. pylori were identified. A deletion study was
performed wherein reactions and associated genes in central
metabolism were deleted and their effects were simulated under
a variety of substrate availability conditions, yielding a
number of reactions that are deemed essential. Deletion results
were compared to recently published in vitro essentiality
determinations for 17 genes. The in silico model accurately
predicted 10 of 17 deletion cases, with partial support for
additional cases. Collectively, the results presented herein
suggest an effective strategy of combining in silico modeling
with experimental technologies to enhance biological discovery
for less characterized organisms and their genomes.
This model is hosted on
BioModels Database
and identified by:
MODEL1507180037.
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2015-07-30 | MODEL1507180037 | BioModels
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Project description:The majority of gastric cancer cases are believed to be caused by chronic infection with the bacterium Helicobacter pylori, and atrophic corpus gastritis is a predisposing condition to gastric cancer development. We aimed to increase understanding of the molecular details of atrophy by performing a global transcriptome analysis of stomach tissue. Biopsies from patients with different stages of H. pylori infection were taken from both the antrum and corpus mucosa and analyzed on microarrays. The stages included patients without current H. pylori infection, H. pylori-infected without corpus atrophy and patients with current or past H. pylori-infection with corpus-predominant atrophic gastritis.Using clustering and integrated analysis, we found firm evidence for antralization of the corpus mucosa of atrophy patients. This antralization harbored gain of gastrin expression, as well as loss of expression of corpus-related genes, such as genes associated with acid production, energy metabolism and blood clotting. The analyses provided detailed molecular evidence for simultaneous intestinal metaplasia (IM) and spasmolytic polypeptide expressing metaplasia (SPEM) in atrophic corpus tissue. Finally, acidic mammalian chitinase, a chitin-degrading enzyme produced by chief cells, was shown to be strongly down-regulated in corpus atrophy.Transcriptome analysis revealed several gene groups which are related to development of corpus atrophy, some of which were increased also in H. pylori-infected non-atrophic patients. Furthermore, loss of acidic chitinase expression is a promising marker for corpus atrophy.
2014-02-04 | GSE27411 | GEO
Project description:The majority of gastric cancer cases are believed to be caused by chronic infection with the bacterium Helicobacter pylori, and atrophic corpus gastritis is a predisposing condition to gastric cancer development. We aimed to increase understanding of the molecular details of atrophy by performing a global transcriptome analysis of stomach tissue. Biopsies from patients with different stages of H. pylori infection were taken from both the antrum and corpus mucosa and analyzed on microarrays. The stages included patients without current H. pylori infection, H. pylori-infected without corpus atrophy and patients with current or past H. pylori-infection with corpus-predominant atrophic gastritis.Using clustering and integrated analysis, we found firm evidence for antralization of the corpus mucosa of atrophy patients. This antralization harbored gain of gastrin expression, as well as loss of expression of corpus-related genes, such as genes associated with acid production, energy metabolism and blood clotting. The analyses provided detailed molecular evidence for simultaneous intestinal metaplasia (IM) and spasmolytic polypeptide expressing metaplasia (SPEM) in atrophic corpus tissue. Finally, acidic mammalian chitinase, a chitin-degrading enzyme produced by chief cells, was shown to be strongly down-regulated in corpus atrophy.Transcriptome analysis revealed several gene groups which are related to development of corpus atrophy, some of which were increased also in H. pylori-infected non-atrophic patients. Furthermore, loss of acidic chitinase expression is a promising marker for corpus atrophy. Biopsies from well classified patients with different stages of H. pylori infection were taken from both the antrum and corpus mucosa. These stages included H. pylori un-infected, H. pylori-infected without corpus atrophy and H. pylori-infected with corpus-predominant atrophic gastritis.
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