Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcript levels in the normal epithelium and adenomas of the colon of Min mice

ABSTRACT: We sought to identify gene transcripts altered in level between the normal epithelium and adenomas in colon of the Apc-Min/+ mouse. These differences in level can be compared to those observed for the colons of the Apc-Pirc/+ rat and the human.

ORGANISM(S): Mus musculus

PROVIDER: GSE107139 | GEO | 2017/11/21

SECONDARY ACCESSION(S): PRJNA419146

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcript levels in the normal epithelium and adenomas of the colon of Min mice

Project description:Transcript levels in the normal epithelium and adenomas of the colon of Min mice

| PRJNA419146 | ENA

Genome-wide mapping of Rad21 binding sites and gene expression profiling in wild type mouse small intestinal epithelial crypts and Apc Min adenomas

Project description:To investigate the role of RAD21 in the transcriptional regulation of global gene expression at early stage of colorectal cancer developments, we peformed the genome-wide analysis to map genomic regions bound by Rad21 in normal small testinal crypts and tumors (adenomas) harvested from Apc Min/+ mice using ChIP-seq. ChIP-seq naalysis identified high confidence RAD21 binding sites unique to normal crypts or adenomas, as well as those common to both tissues. We further performed RNA-seq to profile the changes in gene expression from normal WT crypts to adenomas at the very early stage of adenomagenesis in the context of Rad21 heterozygous loss. mRNA profiles of normal small intestinal crypts (WT) and adenomas from Apc Min/+ and Apc Min/+:Rad21+/- double mutant mouse; Mapping of Rad21 genomic binding sites in normal intestinal crypts (WT) and Apc Min/+ adenomas

2014-10-31 | E-GEOD-59283 | biostudies-arrayexpress

Genome-wide mapping of Rad21 binding sites and gene expression profiling in wild type mouse small intestinal epithelial crypts and Apc Min adenomas

2014-10-31 | GSE59283 | GEO

RNA-Seq of adenomas from Apc-Min mice with additional Tet1 and Tdg mutations

Project description:RNA-Seq of adenomas from Apc-Min mice with additional Tet1 and Tdg mutations

| PRJNA744146 | ENA

DNA methylation of adenomas from Apc-Min mice with additional Tet1 and Tdg mutations

Project description:DNA methylation of adenomas from Apc-Min mice with additional Tet1 and Tdg mutations

| PRJNA743221 | ENA

Transcription profiling of transition from normal intestinal epithelia to adenomas and carcinomas in the APC(Min/+) mice to identify differentially expressed transcripts.

Project description:Transcriptional Profiling of the Transition from Normal Intestinal Epithelia to Adenomas and Carcinomas in the APC(Min/+) Mouse. Samples used in analysis:; * GSM6191-GSM6196 (WT): Ilea epithelial cells from C57/BL6 wild-type samples; * GSM6197-GSM6201 (Adenoma): Epithelial cells from crypts of adenomas of APC(Min/+) mice; * GSM6202-GSM6206 (Carcinoma): Epithelial cells from crypts of carcinomas of APC(Min/+) mice; Using a PixCell IIe instrument (Arcturus), ~30,000 laser firings per sample were used to collect cells of interest. RNA was extracted from captured cells by PicoPure (Arcturus) technique, followed by 2 rounds of RiboAmp amplification (Arcturus), with incorporation of biotinylated nucleotides (Enzo) in the IVT of round 2. All protocols were as per manufacturers instructions. 15ug of labeled cRNA from individual samples were hybridized to respective MG_U74Av2 chips (Affymetrix) and washed/stained using the standard EukGEWS2v4 protocol (Affymetrix). Chips were scanned and analyzed using MAS 5 (Affymetrix) and data scaled to TI=500. Pairwise comparisons using the Mann-Whitney test were performed in DMT 3 (Affymetrix), comparing WT vs Adenoma (n=6 x n=5; 83.3% concordance); WT vs Carcinoma (n=5 x n=5; 84% concordance); Adenoma vs Carcinoma (n=5 x n=5; 84% concordance). This resulted in the identification of differentially expressed transcripts. Fold changes were calculated from signal-log-ratios. Identified transcripts were clustered based on functional information which was publicly available at time of analysis, obtained through the NetAffx web portal (Affymetrix).

2007-11-06 | E-GEOD-422 | biostudies-arrayexpress

Differential Chemopreventive Activity of Sulindac and/or Atorvastatin in Apc+/Min-FCCC Mice With or Without Colorectal Adenomas

Project description:Emerging data suggest that some high-risk subjects benefit more than others from preventive intervention. The goal of this study was to determine the efficacy of sulindac (Sul) and/or atorvastatin (Atorva) against spontaneous colorectal adenomas in Apc+/Min-FCCC mice in which the tumor-bearing status was known at the time of treatment initiation. Administration of Sul/Atorva to tumor-bearing mice led to a 43% reduction in the multiplicity of colorectal adenomas as compared to that of untreated tumor-bearing mice. Atorvastatin completely inhibited the formation of microadenomas in mice that were tumor-free at baseline, with associated decreases in the expression of inflammatory mediators observed. Expression of Hoxb13 and Rprm was enhanced significantly following Sul/Atorva treatment, suggesting the importance of cell cycle regulation in colon tumor inhibition. The tumor status of animals at treatment initiation dictates response to atorvastatin, sulindac and Sul/Atorva. The tumor inhibition observed with Sul/Atorva in tumor-bearing mice was greater than that achieved with either agent alone.

2018-08-31 | GSE81375 | GEO

DNA copy number changes in colorectal flat adenomas

Project description:Background & aim: Flat adenomas form a specific phenotype of colorectal adenomas that has been associated with more severe molecular changes and consequently a more aggressive clinical behavior compared to their polypoid counterparts. In the present study we set out to compare one of the molecular changes most explicitly associated with adenoma to carcinoma progression, i.e. chromosomal instability, between flat and polypoid colorectal adenomas. Methods: Consecutive series of 83 flat and 35 polypoid adenomas were analyzed for DNA copy number changes using a high resolution arrayCGH platform as well as for mutations in the adenomatous polyposis coli (APC) gene. Gene ontology on the genes located on the significantly different regions was performed. Results: Overall, flat adenomas show similar DNA copy number changes as polypoid adenomas. Patterns of DNA copy number changes differed between the two phenotypes with significantly more frequently loss of 5q14.3 and 5q15-q23.3 in flat adenomas, while loss of 1p36.32-p35.3, 10q25.2-q25.3, 17p12 and chromosome 18 were more frequent in polypoid adenomas. The 5q15-q23.3 region harbors the APC locus, therefore mutation status of APC was investigated, showing significantly less mutations in flat adenomas. Pathway analysis and datamining linked the 5q region to inflammation. Conclusion: These results provide evidence that flat and polypoid adenomas have partly overlapping DNA copy number changes, while alterations more specific to flat adenomas have associations with inflammation. Loss of 5q has been associated with aggressive behavior and this could serve as an explanation for a more aggressive clinical behavior of flat lesions.

2012-10-04 | GSE30479 | GEO

Transcriptional profiling of SI adenomas in Apc floxed mice

Project description:Small intestinal adenomas in mice with Apc deficiency following tamoxifen-induced genetic recombination.

2021-02-19 | GSE167008 | GEO

Epithelium transition profile

Project description:Transcriptional Profiling of the Transition from Normal Intestinal Epithelia to Adenomas and Carcinomas in the APC(Min/+) Mouse. Samples used in analysis: * GSM6191-GSM6196 (WT): Ilea epithelial cells from C57/BL6 wild-type samples * GSM6197-GSM6201 (Adenoma): Epithelial cells from crypts of adenomas of APC(Min/+) mice * GSM6202-GSM6206 (Carcinoma): Epithelial cells from crypts of carcinomas of APC(Min/+) mice Using a PixCell IIe instrument (Arcturus), ~30,000 laser firings per sample were used to collect cells of interest. RNA was extracted from captured cells by PicoPure (Arcturus) technique, followed by 2 rounds of RiboAmp amplification (Arcturus), with incorporation of biotinylated nucleotides (Enzo) in the IVT of round 2. All protocols were as per manufacturers instructions. 15ug of labeled cRNA from individual samples were hybridized to respective MG_U74Av2 chips (Affymetrix) and washed/stained using the standard EukGEWS2v4 protocol (Affymetrix). Chips were scanned and analyzed using MAS 5 (Affymetrix) and data scaled to TI=500. Pairwise comparisons using the Mann-Whitney test were performed in DMT 3 (Affymetrix), comparing: * WT vs Adenoma (n=6 x n=5; 83.3% concordance) * WT vs Carcinoma (n=5 x n=5; 84% concordance) * Adenoma vs Carcinoma (n=5 x n=5; 84% concordance) This resulted in the identification of differentially expressed transcripts. Fold changes were calculated from signal-log-ratios. Identified transcripts were clustered based on functional information which was publicly available at time of analysis, obtained through the NetAffx web portal (Affymetrix). Keywords = colon cancer Keywords = gene expression Keywords = DNA microarrays Keywords = beta-catenin Keywords = familial adenomatous polyposis Keywords: ordered

2003-09-12 | GSE422 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data