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Dynamic changes in liver 5-hydroxymethylcytosine profiles upon non-genotoxic carcinogen exposure [Replicated control vs. pb treated study]

ABSTRACT: Dynamic changes in the mouse liver DNA methylome associated with short (1 day) and prolonged (7, 28 and 91 days) exposure to the rodent liver non-genotoxic carcinogen (NGC), phenobarbital (PB).

ORGANISM(S): Mus musculus

PROVIDER: GSE45465 | GEO | 2013/03/25

SECONDARY ACCESSION(S): PRJNA194090

REPOSITORIES: GEO

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Dynamic changes in liver 5-hydroxymethylcytosine profiles upon non-genotoxic carcinogen exposure [Replicated control vs. pb treated study]

Project description:Dynamic changes in the mouse liver DNA methylome associated with short (1 day) and prolonged (7, 28 and 91 days) exposure to the rodent liver non-genotoxic carcinogen (NGC), phenobarbital (PB). Full expression dataset (all time points: 1, 7, 28, 91 days) Replicated control vs. pb treated study

2013-03-25 | E-GEOD-45465 | biostudies-arrayexpress

Dynamic changes in liver 5-hydroxymethylcytosine profiles upon non-genotoxic carcinogen exposure

Project description:29-32 days old male mice where either treated with Phenobarbital or untreated Replicated control vs. pb treated study

2012-09-12 | E-GEOD-40773 | biostudies-arrayexpress

IP of 5-hydroxymethylcytosine (5-hmC) enriched DNA fragments from control ,PB treated mouse livers , resulting Ctnnb1 mutated PB liver tumours and PB minus Ha-Ras mutate liver tumour

Project 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. 5-hmC is a novel epigenetic mark derived from oxidation of methylcytosine. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5hmC in both control mouse livers as well as in the livers of 12 week PB treated mice. We also profile 5hmC in liver tumours arising in the presence of long term PB exposure (35 week: resulting in Ctnnb1 mutated tumours) to a Ha-Ras liver tumour which arose without PB. Samples: 5hmC profiles in 2 control and 2 PB exposed mouse livers, 3 liver tumours resulting from long term PB exposrue and 1 liver tumour arising without PB

2016-05-17 | E-GEOD-77726 | biostudies-arrayexpress

Dynamic changes in liver 5-hydroxymethylcytosine profiles upon non-genotoxic carcinogen exposure

Project description:29-32 days old male mice where either treated with Phenobarbital or untreated

2012-09-12 | GSE40773 | GEO

Trancriptomic profiling of hepatocytes and mesenchymal cells of mice treated with phenobarbital for 2 weeks

Project description:Conventional notion regards the action of non-genotoxic carcinogens (NGC) an autonomous process largely confined to parenchymal cells. Here we aim to elucidate the role of the hepatic mesenchyme for the action of a prototypical NGC, phenobarbital (PB), an anti-epileptic drug.

2017-07-12 | GSE68111 | GEO

Trancriptomic profiling of hepatocytes and mesenchymal cells of rats treated with nongenotoxic carcinogens for up to 2 weeks

Project description:Conventional notion regards the action of non-genotoxic carcinogens (NGC) an autonomous process largely confined to parenchymal cells. Here we aim to elucidate the role of the hepatic mesenchyme for the action of two prototypical NGC, phenobarbital (PB), an anti-epileptic drug, and cyproterone acetate (CPA) a gestagen used in contraceptive pills.

2017-07-12 | GSE68120 | GEO

IP of 5-methylcytosine (5-mC) enriched DNA fragments from control and PB treated mouse livers (91 day)

Project description:5-mC is an epigenetic modification of the DNA base cytosine with roles in gene silencing events, imprinting and X inactivation. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5mC in both control mouse livers as well as in the livers of 91 day PB treated mice. 5mC is largely found to reside in the bodies of active genes and promoter levels are perturbed upon PB induced gene activation events. 5-mC is assocated with promoters fo silent genes. Upon PB exposire a handfull of genes are induced which reveal decreases in promoter 5mC levels

2012-11-10 | GSE41398 | GEO

IP of 5-methylcytosine (5-hmC) enriched DNA fragments from control and PB treated mouse livers (91 day)

Project description:5-hmC is an epigenetic modification of the DNA base cytosine with roles in gene silencing events, imprinting and X inactivation. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5hmC in both control mouse livers as well as in the livers of 91 day PB treated mice. 5hmC is largely found to reside in the bodies of active genes and promoter levels are perturbed upon PB induced gene activation events. 5-hmC is assocated with promoters fo silent genes. Upon PB exposire a handfull of genes are induced which reveal decreases in promoter 5hmC levels

2012-11-10 | GSE41397 | GEO

IP of 5-methylcytosine (5-mc) enriched DNA fragments from control, PB treated mouse livers, resulting Ctnnb1 mutated PB liver tumours and PB minus Ha-Ras mutate liver tumour

Project 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. 5-mc is a well establisehd epigenetic mark typically related to gene silencing events. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5mC in both control mouse livers as well as in the livers of 12 week PB treated mice. We also profile 5mC in liver tumours arising in the presence of long term PB exposure (35 week: resulting in Ctnnb1 mutated tumours) to a Ha-Ras liver tumour which arose without PB. Samples: 2 control and 2 PB exposed mouse livers, 3 liver tumours resulting from long term PB exposrue and 1 liver tumour arising without PB

2016-05-17 | E-GEOD-77727 | biostudies-arrayexpress

IP of 5-hydroxymethylcytosine (5-hmC) enriched DNA fragments from control and PB treated mouse livers (28 day)

Project description:5-hmC is a novel epigenetic mark derived from oxidation of methylcytosine. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5hmC in both control mouse livers as well as in the livers of 28 day PB treated mice. 5hmC is largely found to reside in the bodies of active genes and promoter levels are perturbed upon PB induced gene activation events. 5-hmC is enriched in the bodies of active genes as well as a subset of TSS regions associated with transcriptional silencing. Upon PB exposire a handfull of genes are induced which reveal increases in promoter 5hmC levels

2012-09-12 | GSE40537 | GEO

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