Ontology highlight
ABSTRACT:
PROVIDER: PRJNA126971 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE21549: Expression profiles of EDTA-dissociated colon epithelial cells of wild-type mice and vil-Cre-Bcl9-/-/Bcl9l-/- mice. GSE21576: Expression profiles of laser dissected colon tumor samples of wild-type mice and vil-Cre-Bcl9-/-/Bcl9l-/- mice Refer to individual Series
2010-09-01 | E-GEOD-21603 | biostudies-arrayexpress
Project description:To assess potential changes in Wnt signaling more comprehensively, EDTA-dissociated colon epithelial cells from three pools of wild-type and Bcl9/Bcl9l-mutant mice were subjected to an exploratory comparative gene expression profiling. Total RNA of three samples of EDTA-dissociated colon epithelial cells of wild-type mice and three samples of vil-Cre-Bcl9-/-/Bcl9l-/- mice, each sample consisting of material of two or three different mice, was collected and resulting amplified cDNA hybridized to Affymetrix Mouse Genome 430 2.0 arrays. Samples are labeled as follows: Genotype_PoolID _UniqueID_NumberOfMice.
2010-09-01 | E-GEOD-21549 | biostudies-arrayexpress
Project description:Expression profiles of laser dissected colon tumor samples of wild-type mice and vil-Cre-Bcl9-/-/Bcl9l-/- mice
| PRJNA129317 | ENA
Project description:Expression profiles of EDTA-dissociated colon epithelial cells of wild-type mice and vil-Cre-Bcl9-/-/Bcl9l-/- mice.
| PRJNA129513 | ENA
Project description:We here performed a proteomics study on the colon tissues of ckmt1 KOIEC or. WT (flox+/+) mice after DSS treatment for 8 days (n=3). KOIEC mice (Ckmt1flox/flox, Vil-Cre) means mice with intestinal epithelial conditional knockout (C57BL/6J). Cre-negative Ckmt1 flox/flox littermates were used as controls. Group 1: DSSCKO (Ckmt1flox/flox, Vil-Cre) Group 2: DSSflox (Cre-negative Ckmt1 flox/flox littermates)
2025-05-07 | PXD057053 | Pride
Project description:To assess potential changes in Wnt signaling more comprehensively, EDTA-dissociated colon epithelial cells from three pools of wild-type and Bcl9/Bcl9l-mutant mice were subjected to an exploratory comparative gene expression profiling.
2010-09-01 | GSE21549 | GEO
Project description:To investigate the impact of ablating Bcl9/Bcl9l on tumorigenesis, 6-8- week-old mice were exposed first to a single dose dimethylhydrazine (DMH, 44 mg/kg body weight), which is metabolized in the liver to carcinogenic azoxymethane (AOM), followed by 7 days oral administration of 2 % dextrane sulfate sodium (DSS) in the drinking water. This regimen results in the emergence of dysplastic adenomas, which progress to differentiated adenocarcinomas that are morphologically similar to human colorectal adenocarcinomas and typically harbor β-catenin stabilizing mutations of GSK3ß phosphorylation sites. Accordingly, these tumors present hallmarks of active Wnt signaling such as accumulation of nuclear β-catenin and expression of Wnt target genes. Total RNA of laser dissected samples from five different tumors each of two wild-type mice and three vil-Cre-Bcl9-/-/Bcl9l-/- mice was collected and resulting amplified cDNA hybridized to Affymetrix Mouse Genome 430 2.0 arrays. Samples are labeled as follows: Genotype_TumorID_MouseID_UniqueID.
2010-09-01 | E-GEOD-21576 | biostudies-arrayexpress
Project description:Testis samples from Alkbh1 wild-type and KO mice
2015-09-15 | E-GEOD-22073 | ExpressionAtlas
Project description:The Runx1 transcription factor plays an important role in tissue homeostasis through its effects on stem/progenitor cell populations and differentiation. The effect of Runx1 on epithelial differentiation of the secretory cell lineage of the colon was recently demonstrated. This study aimed to examine the role of Runx1 in tumor development in epithelial cells of the gastrointestinal tract. Conditional knockout mice were generated that lacked Runx1 expression in epithelial cells of the GI tract. These mice were crossed onto the ApcMin background, sacrificed, and their intestinal tumor phenotypes were compared with ApcMin Runx1 wildtype control mice. Apc-wildtype Runx1-mutant mice were also examined for tumor development. Colons from Runx1 knockout and wildtype mice were used for genome-wide mRNA expression analyses followed by gene-specific quantitative RT-PCR of whole colon and colon epithelium, to identify Runx1 target genes. Runx1 deficiency in intestinal epithelial cells significantly enhanced tumorigenesis in ApcMin mice. Notably, epithelial Runx1 deficiency in Apc-wildtype mice was sufficient to cause tumor development. Absence of Runx1 was associated with global changes in expression of genes involved in inflammation and intestinal metabolism, and with gene sets indicative of metastatic phenotype and poor prognosis. Gene-specific analysis of Runx1 deficient colon epithelium revealed increased expression of genes linked to an expansion of the stem/progenitor cell population. These results identify Runx1 as a novel tumor suppressor gene for gastrointestinal tumors and support a role for Runx1 in maintaining the balance between the intestinal stem/progenitor cell population and epithelial differentiation of the GI tract. A total of 8 colon tissue RNA samples were analyzed, comprising 4 colon samples from wild-type mice (Villin-Cre negative / Runx1-floxed) and 4 colon samples from mice that lack epithelial expression of Runx1 (Villin-Cre positive/Runx1-floxed).
2012-09-13 | E-GEOD-34292 | biostudies-arrayexpress
Project description:RNA-seq of 54 samples (normal colon, primary tumor, and liver metastases) from 18 colorectal cancer patients
2025-01-24 | E-GEOD-50760 | ExpressionAtlas