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PROVIDER: PRJNA383939 | ENA |
REPOSITORIES: ENA
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Project description:Genomic and Epigenomic Profiling of High-Risk Intestinal Metaplasia Reveals Molecular Determinants of Gastric Cancer Progression
| PRJNA400467 | ENA
Project description:Metaplasia of the gastric epithelia (intestinal metaplasia, IM) is a pre-malignant lesion associated with increased gastric cancer (GC) risk.
2018-01-09 | GSE103186 | GEO
Project description:Intestinal metaplasia (IM), precancerous lesions of gastric carcinoma (PLGC) induced by factors like nitrite, Helicobacter pylori, or bile acid, carries a high risk of progressing to gastric cancer. IM is categorized into complete intestinal metaplasia (CIM) and incomplete intestinal metaplasia (IIM). Patients with IIM are at a higher risk of developing gastric cancer, emphasizing its importance for early screening. Besides the diagnostic challenges, the mechanisms underlying its progression remain a mystery. OLFM4, a gene associated with stemness characteristics, has been linked to promoting gastric and colorectal cancers. Our investigation used pathological sections from two clinical centers, biopsies of IM tissues, PLGC cell models, animal models, and organoids to explore OLFM4's role in IIM. OLFM4 expression was observed highly in IIM, with superior diagnostic accuracy of IIM compared to CDX2 and MUC2 for the first time. OLFM4, along with MYH9, was highly expressed in IM organoids and PLGC animal models. OLFM4, in combination with MYH9, accelerated the ubiquitination of GSK3β and resulted in increased β-catenin levels through the Wnt signaling pathway, finally promoting the proliferation and invasion abilities of PLGC cells. In conclusion, OLFM4 serves as a novel biomarker for IIM and is utilized as an important auxiliary means to delimit the key population for early gastric cancer screening. This study provides new insights into the mechanisms of progression and a new target of therapy in intestinal metaplasia.
2024-01-01 | GSE251765 | GEO
Project description:Background: Intestinal metaplasia (IM) is a gastric precancerous lesion that precedes the development of gastric cancer in up to 3.77 cases/1000 person-years. It consists in a trans-differentiation process of gastric to intestinal tissue. Two histological subtypes exist, complete (CIM) and incomplete (IIM), the latter having higher progression rates to gastric cancer . Our objective was to identify molecular processes responsible for the tumoral transition from intestinal metaplasia to GC and the initial steps of this lesion Methods: We used expression microarray to compare the transcriptome of intestinal metaplasia subtypes that progress to gastric cancer (IIM-GC and CIM-GC) after a follow-up period with respect to those that do not progress (IIM control and CIM control). Also, IM-NoGC (IM control, comprising both IIM and CIM Control) was compared with healthy gastric mucosa. Differentially expressed genes were obtained and functional analyses (GSEA and IPA softwares) were performed. Some deregulated genes were validated by qPCR. Results: Histological subtypes of intestinal metaplasia that progress or not to GC differ less among them than to healthy mucosa. Incomplete intestinal metaplasia has a higher number of over-expressed carcinogenic genes and molecular processes than the complete subtype. Most relevant molecular processes and genes in this group include antigenic processing, inflammation, activation of cell cycle and cell proliferation, oncogenes and tumor suppressors. When IM-NoGC is compared with healthy gastric mucosa new identified transcripts include TRIM, TMEM, homeobox, transporters and nucleolar RNAs SNORDs116. We confirm previously reported processes such us intestinal differentiation, metabolism of lipids and of xenobiotics and identify new ones such as non tumoral Warburg effect and melatonin degradation. Conclusions: Differentially expressed genes and molecular processes have been identified for the first time in intestinal metaplasia that progress to gastric cancer. New genes and molecular processes have also been identified in intestinal metaplasia in comparison with healthy gastric mucosa.
2017-06-12 | GSE78523 | GEO
Project description:To test the hypothesis that there is a specific miRNA expression signature which characterizes Barrett's esophagus development and progression, we performed miRNA microarray analysis comparing normal esophageal squamous epithelium with the two different metaplastic lesions occuring within Barrett's mucosa (i.e. gastric metaplasia and intestinal metaplasia). Samples of H. pylori-related gastritis and gastric intestinal metaplasia were also considered in the definition of esophageal-specific miRNAs. miRNA microarray analysis was performed in a series of samples obtained from (a) 10 histologically-proven long-segment Barrett's esophagus patients; (b) 10 patients with H. pylori-related chronic atrophic gastritis. Overall, 10 normal esophageal squamous epithelium samples, 10 esophageal intestinal metaplasia samples, 10 esophageal gastric metaplasia samples, 10 H. pylori -related gastritis samples (no atrophic lesion detected; obtained from the antrum) and 10 gastric intestinal metaplasia samples (obtained from the antrum) were considered.
2011-01-01 | E-GEOD-24839 | 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
Project description:To test the hypothesis that there is a specific miRNA expression signature which characterizes Barrett's esophagus development and progression, we performed miRNA microarray analysis comparing normal esophageal squamous epithelium with the two different metaplastic lesions occuring within Barrett's mucosa (i.e. gastric metaplasia and intestinal metaplasia). Samples of H. pylori-related gastritis and gastric intestinal metaplasia were also considered in the definition of esophageal-specific miRNAs.
2011-01-01 | GSE24839 | GEO
Project description:miRNA expression profiles in the progression of the gastric cancer According to the development of intestinal gastric cancer(GC), the normal gastric mucosa gradually evolves into gastric cancer through CSG(Chronic superficial gastritis), CAG(Chronic atrophic gastritis), IM (intestinal metaplasia) and Dys(Dysplasia). H. pylori is the main risk factor for GC, but the mechanism is still unclear. In this study, we indentified the miRNA, lncRNAs and mRNAs expression profiles in GC progression, analyzed the fuctions and pathways and investigated the relationship between non coding RNAs and H. pylori infection. Our study provided new ideas for the study of the pathogenesis of GC and a basis for the early diagnosis and treatment of GC and precancerous lesions.
2023-12-17 | GSE163747 | GEO
Project description:Foregut Microbiome and Risk of Gastric Intestinal Metaplasia, and Gastric Cancer Risk
| PRJNA756701 | ENA