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Expression data from mouse gastric tumor models

ABSTRACT: Transgenic mice with prostaglandin E2 pathway in stomach develops gastric tumors. Simultaneous activation of both Wnt pathway and prostaglandin E2 pathway causes gastric adenocarcinoma. Combination of prostaglandin E2 pathway activation and suppression of BMP pathway leads to the development of gastric hamartomas. We used microarrays to find the mechanism of these tumor development and to evaluate whether these mouse models recapitulate human gastric tumors. Glandular stomach from three C57BL/6 wild-type, five K19-Wnt1 transgenic, three K19-C2mE, five K19-Wnt1/C2mE, two K19-Nog, and three K19-Nog/C2mE transgenic mice were used. All mice were female at 18-65 weeks of age.

ORGANISM(S): Mus musculus

SUBMITTER: Hiraku Itadani

PROVIDER: E-GEOD-16902 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Mouse gastric tumor models with prostaglandin E2 pathway activation show similar gene expression profiles to intestinal-type human gastric cancer.

Itadani Hiraku H Oshima Hiroko H Oshima Masanobu M Kotani Hidehito H

BMC genomics 20091217

<h4>Background</h4>Gastric cancers are generally classified into better differentiated intestinal-type tumor and poorly differentiated diffuse-type one according to Lauren's histological categorization. Although induction of prostaglandin E2 pathway promotes gastric tumors in mice in cooperation with deregulated Wnt or BMP signalings, it has remained unresolved whether the gastric tumor mouse models recapitulate either of human gastric cancer type. This study assessed the similarity in expressio ...[more]

PMID: 20015407

Similar Datasets

Expression data from mouse gastric tumor models

Project description:Transgenic mice with prostaglandin E2 pathway in stomach develops gastric tumors. Simultaneous activation of both Wnt pathway and prostaglandin E2 pathway causes gastric adenocarcinoma. Combination of prostaglandin E2 pathway activation and suppression of BMP pathway leads to the development of gastric hamartomas. We used microarrays to find the mechanism of these tumor development and to evaluate whether these mouse models recapitulate human gastric tumors.

2009-07-02 | GSE16902 | GEO

Hyperplastic gastric tumor of K19-C2mE transgenic mouse

Project description:Cyclooxygenase-2 (COX-2), the rate-limiting enzyme for prostanoid biosynthesis, plays a key role in gastrointestinal carcinogenesis. Among various prostanoids, prostaglandin E2 (PGE2) appears to be most responsible for cancer development. To investigate the role of PGE2 in gastric tumorigenesis, we constructed transgenic mice simultaneously expressing COX-2 and microsomal prostaglandin E synthase (mPGES)-1 in the gastric epithelial cells. The transgenic mice developed metaplasia, hyperplasia and tumorous growths in the glandular stomach with heavy macrophage infiltrations. Although gastric bacterial counts in the transgenic mice were within the normal range, treatment with antibiotics significantly suppressed activation of the macrophages and tumorous hyperplasia. Importantly, the antibiotics treatment did not affect the macrophage accumulation. Notably, treatment of the transgenic mice with lipopolysaccharides induced proinflammatory cytokines through Toll-like receptor 4 in the gastric epithelial cells. These results indicate that an increased level of PGE2 enhances macrophage infiltration, and that they are activated through epithelial cells by the gastric flora, resulting in gastric metaplasia and tumorous growth. Furthermore, Helicobacter infection upregulated epithelial PGE2 production, suggesting that the COX-2/mPGES-1 pathway contributes to the Helicobacter associated gastric tumorigenesis. Keywords: disease state analysis

2006-02-01 | GSE3903 | GEO

Gene expression analysis of three tumor organoids (GAN-WT, GAN-p53 and GAN-KP) derived from gastric tumor in K19-Wnt1/C2mE (GAN) mouse.

Project description:To develop a syngeneic mouse model of metastatic gastric cancer, we established the tumor organoids from gastric tumor arising in GAstric Neoplasia (GAN) mice (GAN-WT) which express Wnt1 and the PGE2 synthesis enzymes COX-2 and microsomal prostaglandin E synthase-1 (mPGES-1) in the stomach epithelium. Furthemore, GAN-WT organoids were genetically manupilated into p53 knockout organoids (GAN-p53KO) and KrasG12V-expressing GAN-p53KO organoids (GAN-KP).

2021-06-15 | GSE178087 | GEO

Spatial transcriptome analysis of gastric cancer which GAN-KP transplanted C57BL/6J mouse

Project description:We have now developed an organoid-based model of gastric cancer from GAstric Neoplasia (GAN) mice, which express Wnt1 and the enzymes COX2 and microsomal prostaglandin E synthase 1 in the stomach. Both p53 knockout (GAN-p53KO) organoids and KRASG12V-expressing GAN-p53KO (GAN-KP) organoids were generated by genetic manipulation of GAN mouse–derived tumor (GAN-WT) organoids. To uncover the molecular mechanism underlying the intratumoral heterogeneity of GAN-KP tumors, we performed spatial transcriptomics analysis with the 10× Genomics Visium platform, which allows characterization of the spatial topography of gene expression.

2021-10-21 | GSE186290 | GEO

Regulation of Parietal Cell Homeostasis by Bone Morphogenetic Protein signaling

Project description:Loss of BMP signaling in the stomach, achieved by transgenic expression of the BMP inhibitor noggin (H+/K+-Nog mice), causes parietal cells (PC) loss, SPEM, a marker of pre-neoplasia, and activation of cell proliferation. Purpose: We examined if specific inhibition of BMP signaling in PCs leads to aberrations in epithelial homeostasis

2023-05-01 | GSE202355 | GEO

A Novel Human Gastric Primary Cell Culture System for Modeling Helicobacter Pylori Infection In Vitro

Project description:We identified specific long-term culture conditions that allow the formation of 3-dimensional human gastric spheroids, which can be differentiated by withdrawal of Wnt3A and R-spondin1 to human gastric organoids. These cultures can expand indefinitely and exhibit important characteristics of human stomach tissue. Furthermore, these 3-dimensional cultures can be transferred into 2-dimensional primary epithelial cell layers, which can be successfully infected with H. pylori and thereby provide ideal conditions to study infections in vitro. Microarray experiments were performed as dual-color hybridizations on Agilent human whole genome catalog 44K arrays. To compensate for dye-specific effects, a dye-reversal color-swap was applied.

2014-12-10 | E-GEOD-58473 | biostudies-arrayexpress

PGE2 promotes recovery from established Nephrotoxic Serum Nephritis in mice.

2012-04-23 | GSE37402 | GEO

Transcriptional profiles of stomach organoids from human embryonic stem cells.

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

PGE2 promotes recovery from established Nephrotoxic Serum Nephritis in mice.

Project description:We induced acute nephritis by single injection of sheep nephrotoxic serum in mice and then treated the mice with prostaglandin E2. We used microarrays to examine the global gene expressions during recovery from nephrotoxic nephritis by prostaglandin E2. Acute nephristis was induced in female mice by single injection of sheep Nephortoxc Serum (NTS), followed by prostaglandin E2 administration daily starting from day 2 after NTS administration. Mice were sacrificed on day 7 and RNAs were isolated from kidney. The RNA samples were subjected to mouse gene 1.0 ST array analysis.

2012-04-22 | E-GEOD-37402 | biostudies-arrayexpress

Signaling through MyD88 in bone marrow-derived cells promotes gastric tumorigenesis by inducing the TLR2/CD14 pathway in tumor cells

Project description:Gan mice express Wnt1, Ptgs2, and Ptges, which develop inflammation-associated gastric tumors (Oshima et al, Gastroenterology 131: 1086, 2006). We examined the role of MyD88 in tumorigenesis by construction of Myd88-/- Gan mice and bone marrow transplantation into Gan mice from Myd88-/- mice. Total RNA was prepared from wild-type normal glandular stomach (n=3: WT 1âWT 3), B6 C2mE mice (n=3: C2mE 1âC2mE 3), B6 Gan mice (n=3: Gan1âGan3), B6 Gan MyD88-/- mice (n=3: Gan 1 (MyD88-/-)âGan 3 (MyD88-/-)), and B6 bone marrow transplanted Gan mice from Myd88-/- mice (n=3: BMT-Gan 1 (from MyD88-/-)âBMT-Gan 3 (from MyD88-/-)). We used Illumina HiSeq 2000, and examined expression profiles.

2015-12-15 | E-GEOD-70135 | biostudies-arrayexpress

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