<HashMap><database>ENA</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR315/002/SRR3157432/SRR3157432.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR315/001/SRR3157431/SRR3157431.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR315/004/SRR3157434/SRR3157434.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR315/003/SRR3157433/SRR3157433.fastq.gz</Fastqsanger.gz></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Genomics</omics_type><center_name>Meehan, MRC Human Genetics Unit, University of Edinburgh</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJNA311320</full_dataset_link><scientific_name>Mus musculus</scientific_name><long_description>Through the analysis of mouse liver tumours promoted by distinct routes (DEN exposure alone, DEN exposure plus non-genotoxic insult with phenobarbital and non-alcoholic fatty liver disease) we report that the cancer associated hyper-methylated CGI events in mice are also predicated by silent promoters that are enriched for both the DNA modification 5-hydroxymethylcytosine (5hmC) and the histone modification H3K27me3 in normal liver. During cancer progression these CGIs undergo hypo-hydroxymethylation, prior to subsequent hyper-methylation whilst retaining H3K27me3. A similar loss of promoter-core 5hmC is observed in Tet1 deficient mouse livers indicating that reduced Tet1 binding at CGIs may be responsible for the epigenetic dysregulation observed during hepatocarcinogenesis. Consistent with this reduced Tet1 protein levels are observed in mouse liver tumour lesions. As in human, DNA methylation changes at CGIs do not appear to be direct drivers of hepatocellular carcinoma progression in mice. Instead dynamic changes in H3K27me3 promoter deposition are strongly associated with tumour-specific activation and repression of transcription. Our data suggests that loss of promoter associated 5hmC in diverse liver tumours licences DNA methylation reprogramming at silent CGIs during cancer progression. Overall design: We carry out Chromatin immunoprecipitation (ChIP) prior to sequencing on Illumina Hiseq 2500 to report on the genome-wide H3K27me3 patterns in normal mouse liver, 12 week Phenobarbital exposed mouse livers and 35 week pehonbarbital exposed liver tumours.</long_description><tag>xref:PubMed:27197233</tag><repository>ENA</repository><description_synonyms>3.4.22.-, Phenylethylbarbiturate, cytoplasmic chromatin, ChIP-Chip, Chromatin Immuno-precipitation, Laboratory, Mus domesticus, 5H)-Pyrimidinetrione, mini-ICE, CLIP-Seq, CASP-14, Assay for Transposase-Accessible Chromatin Using Sequencing, PHENYLETHYLMALONYLUREA, PRO2286, House Mouse, prevention, jecur, Histone H2b, Histone H2a, Phenylethylbarbituric Acid, Phenobarbital Sodium, House, Mesc, Chromatin Immunoprecipitation Sequencing-Chip, Mus musculus domesticus, 2, phenobarbital, 6-trione, 4, Phenylethylbarbitursaeure, Catnb, ctnnb, prevention and control, Mice, Chromatins, Histone H3.3, Chromatin Immunoprecipitation Sequencing Chip, Chromatin Immuno precipitation Sequencing, ctnnb1, reference sample, Swiss, ChIP, Chromatin Immunoprecipitation Paired End Tag, Chromatin Immuno Precipitation Paired End Tag, Monosodium Salt, Phenylbarbital, Cross-Linking and Immunoprecipitation Followed by Deep Sequencing, iecur, 5-Phenyl-5-ethylbarbituric acid, Hysteps, Swiss Mice, 5-ethyl-5-phenyl-2, Sequencing, Chromatin Immunoprecipitation Paired-End Tag, preventive measures, Phenobarbitol, extruding from, OK/SW-cl.35, Phenemal, 5H)-pyrimidinetrione, chromosome scaffold, ATAC-Seq, Chromatin Immunoprecipitation Sequencing-Chips, Histone H5, 6(1H, Histone H4, Histone H7, 3H, Histone H1, Histone H3, Controlled, Bfc, nuclear chromatin, HITS-CLIP, High Throughput Sequencing of RNA Isolated by Crosslinking Immunoprecipitation, Controlling, preventive therapy, exits through, Cross Linking and Immunoprecipitation Followed by Deep Sequencing, CASP14, mouse, ChIP Sequencing, armadillo, ChIP-PET, Histone, ChIP-Exo, beta-catenin, CTNNB, Phenobarbituric Acid, Gardenal, Mus, Mini-ICE, Phenobarbital, Sodium, High-Throughput Sequencing of RNA Isolated by Crosslinking Immunoprecipitation, Phenylaethylbarbitursaeure, Mus musculus, 5-ethyl-5-phenyl-, Acid, MRD19, Luminal, Caspase-14 subunit p10, prophylaxis, mice, Tails, 5-Ethyl-5-phenylbarbituric acid, Swiss Mouse, 5-Ethyl-5-phenyl-pyrimidine-2, 5H)-trione, Chromatin Immunoprecipitation, House Mice, Caspase-14 subunit p19, Phenylethylbarbituric, Chromatin Immuno-precipitation Sequencing, ChIP Exonuclease, exposed, MICE, ChIP-Seq, Histone H1(s), Assay for Transposase Accessible Chromatin Using Sequencing, Laboratory Mice, domesticus, Livers, 5-ethyl-5-phenylpyrimidine-2, Monosodium Salt Phenobarbital, control, ChIA-PET., Chromatin Immuno-Precipitation Paired-End Tag, Mouse, Phenylethylmalonylurea, other neoplasm, ChIP-Exonuclease, Laboratory Mouse, Phenobarbitone</description_synonyms><name_synonyms>Mus musculus, Laboratory Mice., House, Mus, Laboratory, Swiss, Mus domesticus, mouse, Mus musculus domesticus, Swiss Mouse, mouse &lt;Mus musculus>, Mouse, House Mice, Swiss Mice, house mouse, Mice, Laboratory Mouse, House Mouse, mice C57BL/6xCBA/CaJ hybrid, domesticus, Mus muscaris</name_synonyms></additional><is_claimable>false</is_claimable><name>Mus musculus</name><description>Chromatin IP for H3 K27me3 modified histone tails in the liver of control mice, Phenobarbital exposed mice and a resulting Ctnnb1 mutated PB liver tumour [ChIP-seq]</description><dates><last_updated>2025-09-24</last_updated><first_public>2016-05-20</first_public></dates><accession>PRJNA311320</accession><cross_references><GEO>GSE77728</GEO><taxon>10090</taxon><PubMed>27197233</PubMed></cross_references></HashMap>