MicroRNA expression data from mouse primary stomach tissues
Ontology highlight
ABSTRACT: We investigated microRNA expression profiles of gastric cancer tissues from Pdx-1-Cre;Cdh1F/+;Trp53F/F;Smad4F/F mice (pChePS_GC) and normal gastric epithelium (NGE) from Pdx1-1-Cre-negative mice. We used microarrays to detail the global microRNA expression underlying gastric carcinogenesis and identified distinct classes of up and down-regulated microRNAs during this process.
Project description:We investigated gene expression profiles of gastric cancer tissues from Pdx-1-Cre;Cdh1F/+;Trp53F/F;Smad4F/F mice (pChePS_GC), gastric cancer tissues from Pdx-1-Cre;Cdh1F/F;Trp53F/F mice (pCP_GC), and normal gastric epithelium (NGE) from Pdx1-1-Cre-negative mice. We used microarrays to detail the global programme of gene expression underlying gastric carcinogenesis and identified distinct classes of up and down-regulated genes during this process.
Project description:The goal of this study is to investigate the molecular mechanisms of LIFR signaling in pancreatic cancer cells isolated from the classical pancreatic ductal adenocarcinoma mouse model KrasLSL-G12D;Tp53f/f;Rosa26LSL-Luc;Pdx1-Cre mice EpCAM+ pancreatic cancer cells were isolated by FACS from pancreatic tumors developed in Lifrf/f;KrasLSL-G12D/+;Trp53f/f;Rosa26LSL-Luc;Pdx1-Cre or LifrWT;KrasLSL-G12D/+;Trp53f/f;Rosa26LSL-Luc;Pdx1-Cre mice respectively and directly lysed for RNA extraction
Project description:This SuperSeries is composed of the following subset Series: GSE27478: Gene expression differences between the pancreatic tissues of Pdx1-Cre;KrasLSL-G12D and Pdx1-Cre;KrasLSL-G12D;IKK2/betaF/F mice GSE33322: Gene expression analysis between the pancreatic tissues of Pdx1-cre;Kras LSL-G12D and Pdx-cre;KrasLSL-G12D;IKK2/beta F/F mice Refer to individual Series
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.
Project description:Purpose: we used next generation sequencing to analyze gene expression profiles of pancreatic tissues from KrasG12D;Pdx1-Cre and miR-301a-/-;KrasG12D;Pdx1-Cre mice treated with caerulein. The goals of this study are to compare the different gene expression profiles of pancreatic tissue between KrasG12D;Pdx1-Cre and miR-301a-/-;KrasG12D;Pdx1-Cre mice treated with caerulein.
Project description:The aim of this experiment was to use global gene expression profiling to identify genes that are differentially expressed in the islets from Pdx1+/- mice compared to islets isolated from Pdx1 +/+ littermates. The Pdx1 null mutation consists of a nuclear targeted _-galactosidase cassette fused in-frame with the N terminus of PDX-1.
Project description:BACKGROUND & AIMS: Gastric cancer is the second most frequent cause of death from cancer in the world, diffuse-type gastric cancer (DGC) exhibiting a poor prognosis. Germline mutations of CDH1, encoding E-cadherin, have been reported in hereditary DGCs, and genetic and/or epigenetic alterations of CDH1 are frequently detected in sporadic DGCs. Genetic alterations of TP53 are also frequently found in DGCs. To examine the synergistic effect of loss of E-cadherin and p53 on gastric carcinogenesis, we established a mouse line in which E-cadherin and p53 are specifically inactivated in the stomach parietal cell lineage. METHODS: We crossed Atp4b-Cre mice with Cdh1loxP/loxP and Trp53loxP/loxP mice, and examined the gastric phenotype of Atp4b-Cre+;Cdh1loxP/loxP;Trp53loxP/loxP mice. RESULTS: Non-polarization of E-cadherin-negative parietal cells and proton pump-negative atypical foci were observed in the transgenic mice. Intramucosal cancers and invasive cancers composed of poorly differentiated carcinoma cells and signet ring cells, which were histologically very similar to those in humans, were found from 6 and 9 months, respectively. Fatal DGCs developed at 100% penetrance within a year, frequently metastasized to lymph nodes, and had tumorigenic activity in immunodeficient mice. Gene expression profiling analyses also revealed that DGCs in the E-cadherin/p53-deficient mice resembled human DGCs. CONCLUSIONS: Our mouse line is the first genetically modified mouse model of DGC and very useful for clarifying the mechanism underlying gastric carcinogenesis, and provides a new approach to the treatment and prevention of DGC because of morphological and biochemical similarities with human DGC. Two-condition experiment, Gastric cancer vs. normal gastric mucosal tissues. Biological replicates: pooled control sample from five normal gastric mucosal tissues, three replicates from diffuse-type gastric cancer.
Project description:Pooled KRC (LSL-KrasG12D; Rb1L/L; Pdx1-Cre: oncogenic Kras and deleted Rb1 in the pancreas) cells derived from 2 month old mice were compared to pooled KC (LSL-KrasG12D; Pdx1-Cre: oncogenic Kras in the pancreas) cells derived from 8 month old mice.