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Whole exome sequencing of DNA purified from colorectal tumors induced by 1% DSS and adjacent colon controls in MLH1-KO mice

ABSTRACT: Whole exome sequencing of DNA purified from colorectal tumors induced by 1% DSS and adjacent colon controls in MLH1-KO mice

PROVIDER: PRJEB47660 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR6800732_1.fastq.gz	Fastqsanger.gz
	ERR6800732_2.fastq.gz	Fastqsanger.gz
	ERR6800733_1.fastq.gz	Fastqsanger.gz
	ERR6800733_2.fastq.gz	Fastqsanger.gz
	ERR6800734_1.fastq.gz	Fastqsanger.gz

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Whole exome sequencing of DNA purified from colorectal tumors induced by 1% DSS and adjacent colon controls in MLH1-KO mice

Project description:In the process of searching for tumor-specific mutations to predict neoantigens for cancer immunotherapy in a Lynch Syndrome mouse model, tumorigenesis was induced with 1% DSS in drinking water. DNA was isolated from tumors and colon tissue separately from 4 MLH1-KO mice using the DNeasy Qiagen kit according to the manufacturer's protocol. Purity of the DNA was confirmed to be very high with the NanoDrop before sending samples to Illumina for next generation sequencing with the Agilent SureSelect XT Mouse All Exon kit. Finally, an analysis was performed in which common tumor-specific mutations were processed through in silico antigen prediction software in NetMHC.

2021-10-02 | E-MTAB-10962 | biostudies-arrayexpress

Colon mucosa of F344 rats: control treated with 5% DSS vs Resveratrol + 5% DSS

Project description:Expression profile of colon mucosa of F344 rats treated with 5% DSS during five days vs colon mucosa of F344 rats pre-treated for 20 days with resveratrol 1mg/kg/day and during the five days of 5% DSS administration Keywords: Inflammation experiment Two conditions experiment, colon mucosa of F344 rats treated 5% DSS for 5d vs colon mucosa of F344 rats pretreated with 1mg/kg/day resv + 5% DSS for 5d. 8 Biological samples for each group

2009-01-27 | E-GEOD-14544 | biostudies-arrayexpress

Methylation profiling of human colon cancer specimens with or without methylation of the MLH1 promoter.

Project description:Expression profile was obtained for GeneChip probe sets among colon cancer specimens with or without the methylation of MLH1 promoter.

2007-08-29 | E-GEOD-2138 | biostudies-arrayexpress

Primary constitutional MLH1 epimutations: a focal epigenetic event [FFPE data sets]

Project description:Background: Constitutional MLH1 epimutations are characterized by monoallelic methylation of the MLH1 promoter throughout normal tissues, accompanied by allele-specific silencing. The mechanism underlying primary MLH1 epimutations is currently unknown. The aim of this study was to perform an in-depth characterization of constitutional MLH1 epimutations targeting the aberrantly methylated region around MLH1 and other genomic loci. Methods: Twelve MLH1 epimutation carriers, 61 Lynch syndrome patients and 41 healthy controls, were analyzed by Infinium Human Methylation 450K beadchip, and targeted molecular techniques were used to characterize the MLH1 epimutation in carriers and their inheritance pattern. Results: No nucleotide or structural variants were identified in-cis on the epimutated allele in ten carriers, in which intergenerational methylation erasure was demonstrated in two, suggesting primary type of epimutation. CNVs outside the MLH1 locus were found in two cases. EPM2AIP1-MLH1 CpG island was identified as the sole differentially methylated region in MLH1 epimutation carriers compared to controls. Conclusion: Primary constitutional MLH1 epimutations arise as a focal epigenetic event at the EPM2AIP1-MLH1 CpG island in the absence of cis-acting genetic variants. Further molecular characterization is needed to elucidate the mechanistic basis of MLH1 epimutations and their heritability/reversibility.

2017-11-28 | GSE107352 | GEO

Primary constitutional MLH1 epimutations: a focal epigenetic event [blood data sets]

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Gene expression profiles in the PhIP/DSS-induced mouse colon tumors and the adjacent normal epithelium controls

Project description:Differentially expressed genes in the PhIP/DSS-induced mouse colon tumors were identified through the mRNA expression profiles of the tumors and the matching controls using the mouse exonic evidence based oligonucleotide (MEEBO) microarray.

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Colon mucosa of F344 rats: control treated with 5% DSS vs Resveratrol + 5% DSS

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mRNAs and miRNAs expression data from AOM/DSS, AOM, DSS and control mouse colon epithelial tissue at day100 when tumor formed in AOM/DSS bearing mice --- miRNA microarray

Project description:To find out which miRNAs are significantly differential expression and potentially involved in the process of inflammation promoting carcinogenesis of colorectal cancer (CRC). We established a colitis-associated CRC (AOM/DSS, Azoxymethane/Dextran sulfate sodium salt) model, colitis (DSS) model and high dose carcinogen (AOM, about 5 times AOM amount given than AOM/DSS model) model. At day 100 when tumor formed in AOM/DSS bearing mice (colitis-associated CRC mice) but no tumor was found in AOM (high dose carcinogen) and DSS model, we employed miRNA microarray as a discovery platform to identify genes with the potential to involve in the progression of CRC promoted by inflammation. 5-7 weeks female BALB/c mice, (1) AOM/DSS group: AOM 12.5mg/kg i.p. at day 1, DSS drinking 5d/21dx3circles from day 5; (2) AOM group: AOM 10mg/kg i.p. 1/weekx6 from day 1; (3) DSS group: DSS drinking 5d/21dx3circles from day 5. The distal colon epithelial tissues were collected at day100 when tumor formed in AOM/DSS bearing mice. The miRNA microarray experiments were performed together.

2013-05-10 | E-GEOD-44983 | biostudies-arrayexpress

DSS Microbiota LC-MS/MS

Project description:In the DSS-induced colitis model, the epithelial damage and resulting inflammation is restricted to the colon, with a potential influence on the microbial composition in the adjacent cecum. Several studies have reported changes of the gut microbiota in the DSS-induced colitis model and other mouse models of IBD. Furthermore, metaproteomics analysis of the gut microbiome in a mouse model of Crohn’s disease demonstrated that disease severity and location are microbiota-dependent, with clear evidence for the causal role of bacterial dysbiosis in the development of chronic ileal inflammation. We have developed a refined model of chronic DSS-induced colitis that reflects typical symptoms of human IBD without a risky body weight loss usually observed in DSS models [Hoffmann et al., submitted]. In this study, we used metaproteomics to characterize the disease-related changes in bacterial protein abundance and function in the refined model of DSS-induced colitis. To assess the structural and functional changes, we applied 16S rRNA gene sequencing and metaproteomics analysis of the intestinal microbiota in three different entities of the intestinal environment, i.e. colon mucus, colon content and cecum content.

2020-03-17 | PXD007220 | Pride

The MLH1 c.-27C>A and c.85G>T variants are borne on a European ancestral haplotype which underlies an autosomal dominant form of MLH1 epimutation.

Project description:Lynch syndrome, caused by germline heterozygous mutations of the DNA mismatch repair genes MLH1, MSH2, MSH6 and PMS2, or deletions affecting the EPCAM gene upstream of MSH2, is characterized by a predisposition to early-onset colorectal and additional extracolonic cancers. An alternative but rare cause of Lynch syndrome is a constitutional epimutation of MLH1, which is characterized by promoter methylation and transcriptional silencing of a single allele in normal tissues. Worldwide, five families with autosomal dominant transmission of a constitutional MLH1 epimutation linked to an MLH1 haplotype with two single nucleotide variants (c.-27C>A and c.85G>T) have been identified. Array-based genotyping using Affymetrix SNP 6.0 data in four of these families revealed a shared haplotype extending across a ≤2.6 Mb region of chromosome 3p22 encompassing MLH1 and additional flanking genes, indicating common ancestry. Genomic DNA from 5 carriers of the c.-27C>A and c.85G>T variants was hybridized on Affymetrix SNP6.0 array according to manufacturer's procedures

2013-04-01 | E-GEOD-45149 | biostudies-arrayexpress

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