Expression data from biopsies with chronic atrophic gastritis and gastric cancer
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ABSTRACT:
PROVIDER: PRJNA478061 | ENA |
REPOSITORIES: ENA
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Project description:Gastric cancer is an important health problem because it is difficult to diagnose and treat in advanced stage. This makes that the prognosis of gastric cancer patients remains scarce. Currently it is known that the cause of gastric cancer is attributed to chronic infection with Helicobacter pylori. Its persistent infection leads to development of chronic atrophic gastritis that is considered as a predecessor stage of intestinal-type gastric cancer. The understanding of the alteration of molecular mechanisms during the early stages of the development of gastric cancer, and the identification of their potential biomarkers can allow a rapid diagnosis that leads to an improvement diagnosis and increase the patient’s prognosis. We analyzed gene expression profiles of patients with chronic atrophic gastritis and gastric cancer through microarray analysis, functional enrichment analysis and validation of gene expression by quantitative PCR. Gene expression profiles in patients with chronic atrophic gastritis showed molecular changes of the gastric mucosa, which leads to intestinal metaplasia and subsequently, gastric cancer. In gastric cancer the gene expression profile showed the stage of tumor progression, the product of these genes are potential biomarkers of early stages of cancer that can be potential therapeutic targets. Accordingly, the transcriptome analysis revealed several gene groups are related to development of chronic atrophic gastritis, some of which were inhibited in gastric cancer patients. The increased expression of CLDN1, CLDN7, OLFM4, c-Myc and MMP-9 genes in chronic atrophic gastritis and gastric cancer point outs to their use as promising biomarkers for the early diagnosis of gastric cancer.
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Project description:This SuperSeries is composed of the following subset Series: GSE16390: Response of gastric epithelial progenitors to H. pylori isolates from Swedish patients with chronic atrophic gastritis 1 GSE16439: Response of gastric epithelial progenitors to H. pylori isolates from Swedish patients with chronic atrophic gastritis 2 Refer to individual Series
2009-10-26 | E-GEOD-16440 | biostudies-arrayexpress
Project description:Helicobacter pylori colonization of the human stomach is a strong risk factor for gastric cancer. To investigate H. pylori-induced gastric molecular alterations, we used a Mongolian gerbil model of gastric carcinogenesis. Histologic evaluation revealed varying levels of atrophic gastritis (a premalignant condition characterized by parietal and chief cell loss) in H. pylori-infected animals, and transcriptional profiling revealed a loss of markers for these cell types. We then assessed the spatial distribution and relative abundance of proteins in the gastric tissues using imaging mass spectrometry and liquid chromatography with tandem mass spectrometry (LC-MS/MS). We detected striking differences in protein content of corpus and antrum tissues. 492 proteins were preferentially localized to the corpus in uninfected animals. The abundance of 91 of these proteins was reduced in H. pylori-infected corpus tissues exhibiting atrophic gastritis compared to infected corpus tissues with non-atrophic gastritis or uninfected corpus tissues; these included numerous proteins with metabolic functions. Fifty proteins localized to the corpus in uninfected animals were diffusely delocalized throughout the stomach in infected tissues with atrophic gastritis; these included numerous proteins with roles in protein processing. Corresponding alterations were not detected in animals infected with a H. pylori ∆cagT mutant (lacking Cag type IV secretion system activity). These results indicate that H. pylori can cause loss of proteins normally localized to the gastric corpus as well as diffuse delocalization of corpus-specific proteins, resulting in marked changes in the normal gastric molecular partitioning into distinct corpus and antrum regions.
2023-12-04 | PXD046333 | Pride
Project description:To investigate the potential mechanism of action of Xianglianhuazhuo formula (XLHZ) in blocking the progression of chronic atrophic gastritis (CAG) to gastric cancer (GC) . The microRNA (miRNA) expression profiles of gastric mucosal tissues were analyzed by high-throughput sequencing.
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Project description:This randomized phase IIb trial studies how well curcumin works in preventing gastric cancer in patients with chronic atrophic gastritis and/or gastric intestinal metaplasia. Curcumin is an antioxidant compound found in plants that may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.
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Project description:We had one goal to perform this study: Atrophic gastritis and atrophic gastritis receivng PEEPA-P5 antrum epithelial Transcriptomes
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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. 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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Project description:Higher incidence of chronic atrophic gastritis (CAG) is generally considered a precancerous lesion of gastric cancer (GC). Therefore, the early diagnosis and treatment of CAG, especially in Tibetan Plateau areas, play an important role in the prevention of GC. The atrophic and non-atrophic gastric mucosal tissue samples from 7 patients with chronic gastritis (CG) and cancer tissue samples from 3 patients with GC were collected. High-throughput sequencing was performed to identify the differentially expressed in lncRNAs, circRNAs, miRNAs, and mRNAs, followed by the construction of competitive endogenous RNA (ceRNA) regulatory networks (lncRNA/circRNA-miRNA-mRNA network) in CAG. Those differentially expressed mRNAs with the same expression trend in both CAG and GC were further identified. Two datasets (GSE153224 and GSE163416), involving data in non-Tibetan Plateau areas, were used to further screen out plateau-specific mRNAs in CAG, followed by identification of the plateau-specific and ferroptosis related mRNAs. GO and KEGG enrichment analysis were performed to investigate the biological functions of plateau-specific mRNAs in CAG. This study may provide useful information for identifying potential biomarkers for the diagnosis of CAG.
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Project description:Higher incidence of chronic atrophic gastritis (CAG) is generally considered a precancerous lesion of gastric cancer (GC). Therefore, the early diagnosis and treatment of CAG, especially in Tibetan Plateau areas, play an important role in the prevention of GC. The atrophic and non-atrophic gastric mucosal tissue samples from 7 patients with chronic gastritis (CG) and cancer tissue samples from 3 patients with GC were collected. High-throughput sequencing was performed to identify the differentially expressed in lncRNAs, circRNAs, miRNAs, and mRNAs, followed by the construction of competitive endogenous RNA (ceRNA) regulatory networks (lncRNA/circRNA-miRNA-mRNA network) in CAG. Those differentially expressed mRNAs with the same expression trend in both CAG and GC were further identified. Two datasets (GSE153224 and GSE163416), involving data in non-Tibetan Plateau areas, were used to further screen out plateau-specific mRNAs in CAG, followed by identification of the plateau-specific and ferroptosis related mRNAs. GO and KEGG enrichment analysis were performed to investigate the biological functions of plateau-specific mRNAs in CAG. This study may provide useful information for identifying potential biomarkers for the diagnosis of CAG.
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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).
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