Human stomach gastric cancer vs dysplasia
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA656072 | ENA |
REPOSITORIES: ENA
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Project description:Non-tumor stomach tissue from gastric cancer patients.
2007-03-27 | E-SMDB-3964 | biostudies-arrayexpress
Project description:Gastric cancers account for the fourth most frequent cancer death worldwide. Although many differential gene expression profiles are reported for gastric cancers, their variation at the post-transcriptional level has not been provided yet. In this study, we compared the gene expressions of normal stomach vs. stomach cancer in an exon-wise manner and compared alternatively spliced transcripts. The RNA from normal and cancer tissues of gastric cancer patients were subjected to Exon 1.0 ST microarrays. Transcriptome analysis of RNAs from normal and cancer tissues of human stomach by exon array. We analyzed 30 pairs of normal-cancer stomach tissues using the Affymetrix Human Exon 1.0 ST platform. Array data was processed by the Affymetrix Exon Array Computational Tool.
2014-07-12 | E-GEOD-30727 | biostudies-arrayexpress
Project description:Gastric cancers account for the fourth most frequent cancer death worldwide. Although many differential gene expression profiles are reported for gastric cancers, their variation at the post-transcriptional level has not been provided yet. In this study, we compared the gene expressions of normal stomach vs. stomach cancer in an exon-wise manner and compared alternatively spliced transcripts. The RNA from normal and cancer tissues of gastric cancer patients were subjected to Exon 1.0 ST microarrays.
2014-07-12 | GSE30727 | GEO
Project description:MicroRNA (miRNA) expression profiles for gastric cancers were examined to investigate the miRNA involvement in stomach carcinogenesis. miRNA microarray analysis identified statistical unique profiles, which could discriminate stomach cancers from noncancerous stomach tissues.
2005-12-31 | E-TABM-50 | biostudies-arrayexpress
Project description:Gastric cancer (GC) is one of the most common malignant cancers in the world. c-Myc, a well-known oncogene, is commonly amplified in many cancers, including gastric cancer. However, it is still not completely understood how c-Myc functions in GC. Here, we generated a stomach-specific c-Myc knock-in mouse model to investigate its role in GC. We found that overexpression of c-Myc in Atp4b+ gastric parietal cells could induce intestinal-type gastric cancer in mice. Mechanistically, c-Myc promoted tumorigenesis via the AKT/mTOR pathway. Furthermore, AKT inhibitor (MK-2206) or mTOR inhibitor (Rapamycin) inhibited the proliferation of c-Myc overexpressing gastric cancer cell lines. Thus, our findings highlight that gastric cancer can be induced by c-Myc overexpression through activation of the AKT/mTOR pathway.
2021-08-11 | GSE145583 | GEO
Project description:stomach microbiome shape in two gastric cancer subtypes
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Project description:Transcriptional profiling of circular RNA in stage III gastric cancer patient: Tumour vs. Normal mucosa tissue
2017-12-14 | GSE83521 | GEO
Project description:We analyzed DNA copy number alterations in 64 human gastric cancer samples and 8 gastric cancer cell lines using bacterial artificial chromosome (BAC) arrays based comparative genomic hybridisation (aCGH). Gastric cancer tumor tissue samples and cell lines vs normal blood samples
2012-11-05 | E-GEOD-33501 | biostudies-arrayexpress
Project description:Spontaneous metastasis of gastric carcinoma to secondary organs is seldom reproduced in the mice. In this study, we established highly reproducible, experimental mice model in which gastric carcinoma progressively grows in the site of gastric walls and metastasize to secondary sites. A highly tumorigenic GC cells were engineered to express type 2 luciferase and injected via orthotopic route into BALB/c nude mice. The mice developed highly progressive GC tumors in the gastric wall where implanted and slow metastases to liver, spleen, lung, kidney and ovary, with rate of metastases to ovary being 63.6% of implanted mice. The tumors colonized in the ovary expressed a GI marker MUC5A, suggestive of typical human Krukenberg tumor. Immuno-histochemical stainings revealed that many mesenchymal markers were strongly positive in motile tumor cells in the vein of ovary and became gradually weak during extravasations to colonize in the ovary. When routes of metastasis were further investigated, the mesenchymal marker SMA stained low in the tumor cells of the primary site of stomach wall, became high in intravasating vein in the stomach wall, remained high in extravasating veins in the liver and ovary and finally returned low in the colonized tumor in the liver and ovary. However, expression of an epithelial marker Claudin did not show in the opposite profile to SMA, indicating that acquisition of mesenchymal phenotypes rather than loss of epithelial characteristics may more give rise to metastatic potential. Dissociated cells derived from tumors in the implanted mouse stomach or metastasized to ovaries retain their tumorigenicity and metastatic potentials. The mRNA microarray and Western blot analyses showed that metastatic tumor-derived cells showed significantly higher expression of GAGE12 gene family than orthotopic tumors-derived cells. The shRNA-mediated knock-down of the GAGE12 family in the metastatic tumors-derived cells abolished the tumor formation in gastric wall and metastasis as well. In conclusion, we established an in vivo orthotopic gastric cancer mouse model spontaneously metastasizing to secondary organs including ovary, which exhibits typical characteristics of a Krukenberg tumor. Expression of mesenchymal markers should be functionally associated with the gain of metastatic ability in this study. A hightly tumorigenic gastric carcinoma SNU-16 cells were orthotpically injected into stomach wall. Tumors formed in the stomach wall (16S) and mestasized to ovary (16O) were dissociated and cultured for 7 day. These cells were re-injected orthotopically and tumors formed in the stomach from 16S (16SS) and ovary from 16O injection (16OO) were dissociated. Total RNAs were isolated from 16S, 16SS, 16O and 16OO2 and subjected to mRNA microarrays
2013-06-01 | E-GEOD-47554 | biostudies-arrayexpress
Project description:Gastric ulcer, which affect many of patients and is deeply related with gastric cancer, is caused by chronic gastric acid stimulation. Stomach fundus, the main body of stomach, is a major source of gastric acid and peptidase for food digestion. Recapturing the main body of stomach requires mainly 3 functionally differentiated cells; parietal (oxyntic) cells, chief (zymogenic) cells, and surface mucous foveolar (pit) cells. We have previously shown the induction of stomach tissue with functional secreting activities by directed differentiation of mouse embryonic stem cells (ES cells) to stomach primordium with both gut epithelium and splanchnic mesoderm. However, generating human stomach with fundus and such functions has been elucidated and a long-desired goal. Here, we describe the method for establishing human embryonic stem cell-derived stomach organoids with fundus gland structure. Along with mouse stomach development and de novo stomach generation from mouse ES cells in vitro, we observed gut-like structure formation from human embryonic stem cells by induction of both endoderm and mesoderm. These human embryonic gut could differentiate into stomach primordium by growth factor stimulation as well as stomach development, and form stomach tissue in three-dimensional organoid culture. Furthermore, these stomach organoids contain fundus-like gland with parietal cells and chief cells, some of secreting activities, and is transcriptionally close to human stomach. Human functional stomach derived from embryonic stem cells represent powerful tools for analying human stomach development, and gastric ulcer related disease including gastric tumorgenesis.
2017-08-31 | GSE79673 | GEO