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Dissecting Expression Profiles of Gastric Precancerous Lesions and Early Gastric Cancer to Explore Crucial Molecules in Intestinal-type Gastric Cancer Tumorigenesis

ABSTRACT: Dissecting Expression Profiles of Gastric Precancerous Lesions and Early Gastric Cancer to Explore Crucial Molecules in Intestinal-type Gastric Cancer Tumorigenesis

PROVIDER: PRJNA541526 | ENA |

REPOSITORIES: ENA

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Dissecting Expression Profiles of Gastric Precancerous Lesions and Early Gastric Cancer to Explore Crucial Molecules in Intestinal-type Gastric Cancer Tumorigenesis

Project description:To investigate the changes in molecular expression, biological processes, stemness, immune microenvironment, tumor hallmark activities and co-expression relationships during intestinal-type gastric cancer carcinogenesis and to excavate the prognostic information contained in the carcinogenesis process. RNA expression profiles of ninety-four gastroscope biopsy samples with different stages of precancerous lesions or early gastric cancers and their paired controls were detected by Agilent Microarray.

2020-03-15 | GSE130823 | GEO

Dissecting expression profiles of gastric precancerous lesions and early gastric cancer to explore crucial molecules in intestinal-type gastric cancer tumorigenesis.

Project description:Intestinal-type gastric cancer (IGC) has a clear and multistep histological evolution. No studies have comprehensively explored gastric tumorigenesis from inflammation through low-grade intraepithelial neoplasia (LGIN) and high-grade intraepithelial neoplasia (HGIN) to early gastric cancer (EGC). We sought to investigate the characteristics participating in IGC tumorigenesis and identify related prognostic information within the process. RNA expression profiles of 94 gastroscopic biopsies from 47 patients, including gastric precancerous lesions (GPL: LGIN and HGIN), EGC, and paired controls, were detected by Agilent Microarray. During IGC tumorigenesis from LGIN through HGIN to EGC, the number of activity-changed tumor hallmarks increased. LGIN and HGIN had similar expression profiles when compared to EGC. We observed an increase in the stemness of gastric epithelial cells in LGIN, HGIN, and EGC, and we found 27 consistent genes that might contribute to dedifferentiation, including five driver genes. Remarkably, we perceived that the immune microenvironment was more active in EGC than in GPL, especially in the infiltration of lymphocytes and macrophages. We identified a five-gene signature from the gastric tumorigenesis process that could independently predict the overall survival and disease-free survival of GC patients (log-rank test: p < 0.0001), and the robustness was verified in an independent cohort (n > 300) and by comparing with two established prognostic signatures in GC. In conclusion, during IGC tumorigenesis, cancer-like changes occur in LGIN and accumulate in HGIN and EGC. The immune microenvironment is more active in EGC than in LGIN and HGIN. The identified signature from the tumorigenesis process has robust prognostic significance for GC patients. © 2020 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

| S-EPMC7317417 | biostudies-literature

Proteomics and Metabolomics unveils Codonopsis Radix ameliorates Gastric Precancerous Lesions via regulating energy metabolism

Project description:Modern pharmacology has proved that Codonopsis Radix and its active ingredients can treat stomach diseases by ameliorating gastrointestinal motility and regulating oxidase levels. However, the detailed molecular mechanism is still unclear. In this study, we systematically evaluated the pharmacodynamic effects of Codonopsis Radix in Gastric Precancerous Lesions animal models. Considering the combination of proteomics and metabolomics, we found that CR could significantly reversed the biological pathways related to energy metabolism which were disturbed by GPL model. Furthermore, the results of serum pharmacology indicated that the Codonopsis Radix contained serum could ameliorate gastritis injury, and selectively inhibit the proliferation of gastric cancer cells rather than normal cells, which was closely related to ATP production in above cells.

2022-10-15 | PXD032714 | Pride

Study on the Effect of Bile Reflux on Gastric Cancer and Its Precancerous Lesions: a Cross-sectional Study.

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Increased expression of Deleted in Malignant Brain Tumors (DMBT1) gene in advanced precancerous gastric lesions in three ethnic populations: effect of modulation on mouse mucous metaplasia in response to H. pylori infection

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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

Expression data from 70 gastric cancer patients

Project description:To explore the spectrum of genetic aberrations of Chinese gastric cancer, 70 samples were further profiled by Affymetrix Hu133Plus2 arrays for mRNA expression 70 gastric cancer frozen tumor tissues were selected for RNA extraction and hybridization on Affymetrix microarrays. All these samples have been also profiled using Agilent 244K array CGH technology.

2014-05-06 | E-GEOD-57303 | biostudies-arrayexpress

H. pylori SlyD Enhances TPT1 Stability via hnRNPK to Promote OCT1-Mediated CDX2 Transcriptional Activation Triggering Gastric Intestinal Metaplasia

Project description:Gastric intestinal metaplasia (GIM) is an important precancerous lesion in intestinal-type gastric cancer, with persistent Helicobacter pylori (H. pylori) infection inducing the condition. In a previous study, we identified a new H. pylori virulence factor, SlyD. However, its mode of action between GIM was unknown. Our findings offer clues to reveal the molecular mechanism of H.pylori infection-associated gastric intestinal metaplasia, and provides the mechanism of a novel H. pylori virulence factor SlyD in gastric precancerous disease.

2024-11-26 | GSE282336 | GEO

Expression profiling on HPSE deleted SGC-7901 gastric cancer cells

Project description:HPSE plays important roles in gastric cancer cell proliferation, apoptosis and metastasis.The aim of this study is to explore molecular mechanism underling roles of HPSE in gastric cancer cell proliferation, survival, migration and metastasis. SGC-7901 gastric cancer cells were transfected with HPSE siRNA (10nM) or scramble control siRNA, RNA were extracted 24hours after transfectioin and hybridized to Affymetrix microarrays. 3 biological repeats were used for each condition.

2013-12-02 | E-GEOD-34080 | biostudies-arrayexpress

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