Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mouse colon tumors compared to normal colon

ABSTRACT: Label-free proteomics from colon tumors induced in C57BL/6J mice following exposure to azoxymethane plus dextran sodium sulfate. Normal colon was taken from age matched mice not exposed to AOM/DSS.

ORGANISM(S): Mus Musculus (mouse)

SUBMITTER: Kelsey Fisher-Wellman

PROVIDER: PXD042677 | JPOST Repository | Mon Jun 03 00:00:00 BST 2024

REPOSITORIES: jPOST

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	1008_WT.raw	Raw
	1014_WT.raw	Raw
	1017_WT.raw	Raw
	1026_WT.raw	Raw
	1030_WT.raw	Raw

Items per page:

1 - 5 of 11

Similar Datasets

Effects of dietary folic acid on methylation status of colon non-neoplastic epithelium and dysplasia in mice with colitis

Project description:Folic acid supplementation (8 mg/kg diet) promotes colon tumor formation in mice with established colitis induced by carcinogen azoxymethane (AOM) and dextran sulfate sodium sulfate (DSS). This induction of colon tumors was associated with hypomethylation of DNA cased by folic acid supplementation.

2023-09-07 | GSE168975 | GEO

Effects of dietary folic acid levles on colitis-associated tumorigenesis.

2023-05-31 | GSE168525 | GEO

Transcriptional profiling of colon cancer tumors in mice with Trim21 gene Knock out

Project description:To investigate the biological function Trim21 in the colon cancer, we compared the gene expression profiles of colon tumor tissues from Trim21 +/+ and Trim21 -/- mice treated with the carcinogen azoxymethane (AOM) and the proinflammatory agent dextran sulfate sodium (DSS).

2025-08-22 | GSE254960 | GEO

Gene expression in the colon of DSS-treated Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice

Project description:Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice are all more sensitive than wild type (WT) mice to dextran sulfate sodium (DSS)-induced colitis. The purpose of this study was to determine which genes are differentially induced by DSS treatment in the colon of Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice compared to WT mice. The results demonstrate higher induction of proinflammatory gene expression in Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice than in WT mice after DSS treatment. The majority of genes whose expression is increased in Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice but not in WT mice are interferon-inducible genes. Thus, Peptidoglycan Recognition Proteins Pglyrp1, Pglyrp2, Pglyrp3, and Pglyrp4 protect mice from excessive inflammatory response and damage to the colon by limiting expression of interferon-inducible genes in the colon.

2010-08-23 | GSE18859 | GEO

Altered epigenetic programming links intestinal inflammation to colon cancer (RNA-seq)

Project description:This study uses whole-transcriptome sequencing to characterize the transcriptomes of the AOM/DSS mouse model. In this model, mice are treated with dextran sodium sulfate (DSS) to induce colitis. When this treatment is preceded by injections of the weak carcinogen azoxymethane (AOM) the mice develop intestinal tumors. Our results identify sets of differentially expressed genes which are correlated with methylation changes of the corresponding genes.

2015-06-17 | GSE57533 | GEO

Reduction of DNA methylation suppresses colon carcinogenesis through induction of tumor cell differentiation

Project description:In this study, we analyzed global gene expressions of colon tumors from DNA hypomethylated and the control mice. We found that DNA hypomethylated tumors express significantly higher levels of intestinal differentiation-related genes when compared with the control tumors. These results suggest that DNA methylation may play a role in the maintenance of undifferentiated state of colon tumor cells. Two different Dnmt1 mutant alleles were used in this study; hypomorphic Dnmt1chip allele and conventional KO Dnmt1c allele, which described previously. Previous studies indicated that Dnmt1chip/c mice have reduced DNA methylation contents at pericentromeric satellite repeats, while Dnmt1chip/+ mice have the same levels of genomic methylation as wildtype mice. Experimental mice in an isogenic F1 hybrid background were obtained by breeding Dnmt1c/+; ApcMin/+ mouse in the C57BL/6 background with Dnmt1chip/chip; Apc+/+ mouse in the 129Sv4 background. Six-week-old DNA hypomethylated (Dnmt1chip/c; ApcMin/+) and the control (Dnmt1chip/+; ApcMin/+) mice were fed with 2% (w/v) dextran sodium sulfate (DSS), a potent promoter for colon carcinogenesis. At 20 weeks of age, colon tumors were harvested from both cohorts (n=3 for both DNA hypomethylated tumors and the control tumors) and analyzed for their gene expressions.

2015-08-05 | E-GEOD-60620 | biostudies-arrayexpress

High-Fat Diet-Induced Liver-Gut Crosstalk Suppresses Autophagy and Exacerbates Colitis [colon]

Project description:The goal of this project is to investigate the mechanisms through which high fat diet (HFD) exacerbates colitis via the liver-gut axis, particularly focusing on liver dysregulated lipid metabolism and intestinal autophagy. We examined colon transcriptomes of C57BL6/J mice fed a control diet (CD) or HFD with or without dextran sulfate sodium (DSS) by RNA seq analysis.

2025-07-02 | GSE293222 | GEO

Expression profiles of colon macrophages from macrophage-specific E4BP4 transgenic mouse [ColonMac_RNA-seq]

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to evaluate the effects of macrophage-specific E4BP4 overexpression under c-fms gene promoter on colon macrophages during the recovery phase of Dextran Sodium Sulfate (DSS)-induced colitis. Methods: We generated transgenic mice (TG) with macrophage-specific E4BP4 overexpression. Colon macrophages were isolated at Zeitgeber Time (ZT) 0 from TG mice and WT littermates and total RNA was extracted. Colon macrophage RNA profiles were generated by deep sequencing for two groups with three mouse samples each. Results: There were significant differences between TG and WT mice. Conclusions: Colon macrophages from the E4BP4 transgenic mice during the recovery phase of DSS-induced colitis might be altered at the transcription level.

2024-03-31 | GSE183075 | GEO

LGR5 positivity defines stem-like cells in colorectal cancer [aCGH]

Project description:Lgr5-EGFP-IRES-Cre-ERT2 mice were exposed to azoxymethane/dextrane sodium sulfate (AOM/DSS) which induces inflammation-driven colon tumors. Tumors were then flow-sorted into fractions of epithelial cells that expressed high or low levels of Lgr5. To exclude that transcriptional differences between Lgr5 high and low mouse colon tumor cells were imposed by distinct patterns of chromosomal aberrations in the two cell fractions, we also performed array comparative genomic hybridization (aCGH) from these tumors. All eight analyzed tumors were chromosomally stable, and thus, no difference between Lgr5 high and low cells could be detected. AOM/DSS-induced mouse colon tumors were flow-sorted into Lgr5 high and low cells before aCGH was performed. Biological replicates: 8. Two CGH array platforms.

2013-05-07 | E-GEOD-46711 | biostudies-arrayexpress

DSS induced colitis mice Astral-DIA

Project description:This study aims to investigate the protein expression profiles in a murine model of dextran sulfate sodium (DSS)-induced colitis using advanced Astral-DIA quantitative proteomics technology. A total of 12 colon tissue samples were analyzed, including 6 from healthy control mice and 6 from DSS-treated mice with induced colitis. Experimental Design Species: Mus musculus (C57BL/6 strain). Tissue Source: Colon tissues were dissected, snap-frozen in liquid nitrogen, and homogenized to extract proteins. Groups: Control Group: Healthy mice without intervention. DSS Group: Mice subjected to 2.5% DSS administration for 7 days to induce colitis, validated by histopathological assessment.

2025-09-18 | PXD063633 | Pride

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