Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Editing of the gut microbiota reduces carcinogenesis in mouse models of colitis-associated colorectal cancer

ABSTRACT: Editing of the gut microbiota reduces carcinogenesis in mouse models of colitis-associated colorectal cancer

PROVIDER: PRJEB29047 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR2822700.fastq.gz	Fastqsanger.gz
	ERR2822710.fastq.gz	Fastqsanger.gz
	ERR2822720.fastq.gz	Fastqsanger.gz
	ERR2822730.fastq.gz	Fastqsanger.gz
	ERR2822740.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

Editing of the gut microbiota reduces carcinogenesis in mouse models of colitis-associated colorectal cancer

Project description:Editing of the gut microbiota reduces carcinogenesis in mouse models of colitis-associated colorectal cancer

| PRJEB32761 | ENA

Editing of the gut microbiota reduces carcinogenesis in mouse models of colitis-associated colorectal cancer.

Project description:Chronic inflammation and gut microbiota dysbiosis, in particular the bloom of genotoxin-producing E. coli strains, are risk factors for the development of colorectal cancer. Here, we sought to determine whether precision editing of gut microbiota metabolism and composition could decrease the risk for tumor development in mouse models of colitis-associated colorectal cancer (CAC). Expansion of experimentally introduced E. coli strains in the azoxymethane/dextran sulfate sodium colitis model was driven by molybdoenzyme-dependent metabolic pathways. Oral administration of sodium tungstate inhibited E. coli molybdoenzymes and selectively decreased gut colonization with genotoxin-producing E. coli and other Enterobacteriaceae. Restricting the bloom of Enterobacteriaceae decreased intestinal inflammation and reduced the incidence of colonic tumors in two models of CAC, the azoxymethane/dextran sulfate sodium colitis model and azoxymethane-treated, Il10-deficient mice. We conclude that metabolic targeting of protumoral Enterobacteriaceae during chronic inflammation is a suitable strategy to prevent the development of malignancies arising from gut microbiota dysbiosis.

| S-EPMC6781011 | biostudies-literature

Tauroursodeoxycholic Acid (TUDCA) Reduces ER Stress and Disease Activity in Ulcerative Colitis

Project description:TUDCA Reduces Ulcerative Colitis Severity

| PRJEB73884 | ENA

Gene expression profiling of proximal versus distal mouse colon during AOM/DSS-induced colitis-associated carcinogenesis.

Project description:In humans with UC, low-grade dysplasia also develops predominantly in the distal colon, progresses more rapidly to neoplasia than proximal colon low-grade dysplasia and associates with worse patient prognosis. In a mouse model of colitis-associated carcinogenesis induced by administration of the mutagen AOM and the luminal toxin DSS, tumors also develop exclusively in the distal part of the large intestine. We monitored global changes in the transcriptome of mouse proximal and distal colon during exposure to AOM/DSS with the aim to define biological pathways and processes that characterize regional responses of the large intestine to colitis-associated carcinogenesis.

2015-06-01 | GSE64658 | GEO

The effect of 5-ASA on colitis-associated carcinogenesis

Project description:The effect of 5-ASA on colitis-associated carcinogenesis

| PRJNA769946 | ENA

Tauroursodeoxycholic Acid (TUDCA) Reduces ER Stress and Lessens Disease Activity in Ulcerative Colitis

Project description:TUDCA Reduces Ulcerative Colitis Severity

| PRJEB73763 | ENA

Thrombospondin 1 in a model of colorectal carcinogenesis

Project description:By using a model of inflammation-induced carcinogenesis the effects of TSP-1 in induced tumors were analyzed. Mice received a single injection of azoxymethane (AOM) and multiple cycles of dextran sodium sulfate (DSS) for inducing chronic inflammation-related cancers. Proliferation and angiogenesis status were analyzed as well as their transcript profile by using a gene microarray approach. We used Affymetrix GeneChips to determine the changes in the genetic profile between WT and TSP-1 deficient tumors in a model of colorectal carcinogenesis. We identified differentially expressed genes between WT and TSP-1 deficient tumors. WT and TSP-1 deficient mice were with a single injection of AOM and were drinking 1.5%DSS (dextran sulfate sodium) to induce colitis in four cycles. Wt mice drinking water only was used as reference. Mice were sacrificed and tumors excised for these studies and morphological analyses

2015-08-26 | E-GEOD-60805 | biostudies-arrayexpress

Blocking TNF-alpha in mice reduces colorectal carcinogenesis associated with chronic colitis.

Project description:The inflammatory bowel disease ulcerative colitis (UC) frequently progresses to colon cancer. To understand the mechanisms by which UC patients develop colon carcinomas, we used a mouse model of the disease whereby administration of azoxymethane (AOM) followed by repeated dextran sulfate sodium (DSS) ingestion causes severe colonic inflammation and the subsequent development of multiple tumors. We found that treating WT mice with AOM and DSS increased TNF-alpha expression and the number of infiltrating leukocytes expressing its major receptor, p55 (TNF-Rp55), in the lamina propria and submucosal regions of the colon. This was followed by the development of multiple colonic tumors. Mice lacking TNF-Rp55 and treated with AOM and DSS showed reduced mucosal damage, reduced infiltration of macrophages and neutrophils, and attenuated subsequent tumor formation. WT mice transplanted with TNF-Rp55-deficient bone marrow also developed significantly fewer tumors after AOM and DSS treatment than either WT mice or TNF-Rp55-deficient mice transplanted with WT bone marrow. Furthermore, administration of etanercept, a specific antagonist of TNF-alpha, to WT mice after treatment with AOM and DSS markedly reduced the number and size of tumors and reduced colonic infiltration by neutrophils and macrophages. These observations identify TNF-alpha as a crucial mediator of the initiation and progression of colitis-associated colon carcinogenesis and suggest that targeting TNF-alpha may be useful in treating colon cancer in individuals with UC.

| S-EPMC2213370 | biostudies-literature

Expression data for the different phases of ulcerative colitis-associated carcinogenesis in a mouse model

Project description:Nonresolving inflammation is correlated to carcinogenesis. Ulcerative colitis-associated colorectal cancer (UC-CRC), one of the typical carcinoma generated by inflammation that cannot be resolved properly, has been widely believed to involve a multistep process contains “inflammation-dysplasia-cancer” sequence. The exact molecular mechanisms underlying the step-wise development of UC-CRC is still not fully understood. Detecting the changes in gene expression profiles may help to reveal why and how does the prolonged inflammatory response lead to carcinogenesis, and to characterize potential diagnostic/prognostic markers or additional therapeutic targets for UC-CRC. There for, we performed temporal genome expression profiling analysis using the Affymetrix genome wide microarray system to identify broad scale changes in gene expression associated with the development of colitis-associated cancer, based on an AOM/DSS induced mouse model of UC-CRC.

2012-08-02 | GSE31106 | GEO

Identification of microRNA landscape of inflammation-induced colorectal carcinogenesis

Project description:Inflammatory conditions can contribute to tumor formation. However, any clear marker predicting progression to cancer are still lacking. The aim of our study was to analyze microRNA modulations accompanying inflammation-induced tumor development to determine whether these microRNA may jointly affect the expression of genes involved in cancer. For this purpose, we used the well-established azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced mouse model of colitis-associated cancer. We performed a microRNA microarray to establish microRNA expression profiles in mouse whole colon at early and late time points during inflammation and/or tumor growth. Chronic inflammation and carcinogenesis were associated with distinct changes in microRNA expression. Nevertheless, prediction algorithms of microRNA-mRNA interactions and computational analyses based on ranked microRNA lists consistently identified putative target genes that play essential roles in tumor growth or belong to key carcinogenesis-related networks or signaling pathways. Hence, inflammation, through microRNA, may affect unexpected genes or signaling pathways, thereby contributing to carcinogenesis. The present method can lead to the identification of novel genes or signaling pathways involved in cancer development. miRNA microarray profiling in whole mouse colon at 4 time points during AOM/DSS treatment. Controls : PBS, DSS alone or AOM alone, at two time points; 10 experimental conditions, 5 replicates per experimental conditions, one replicate per array hybridized in dual color with a commercial reference (Universal Reference, Miltenyi Biotec GmbH)

2013-12-31 | E-GEOD-38443 | biostudies-arrayexpress

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