Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA174865 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE40537: IP of 5-hydroxymethylcytosine (5-hmC) enriched DNA fragments from control and PB treated mouse livers GSE40538: IP of 5-methylcytosine (5-mC) enriched DNA fragments from control and PB treated mouse livers GSE40773: Dynamic changes in liver 5M-bM-^@M-^P hydroxymethylcytosine profiles upon nonM-bM-^@M-^P genotoxic carcinogen exposure Refer to individual Series
2012-09-12 | E-GEOD-40540 | biostudies-arrayexpress
Project description:Dynamic changes in liver 5-hydroxymethylcytosine profiles upon non-genotoxic carcinogen exposure [Replicated control vs. pb treated study]
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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).
2013-03-25 | GSE45465 | GEO
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
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 liver tumours of high fat diet exposed mice who have progressed through NASH. Samples: 5mC profiles in livers of 2 control and 2 NASH driven HCC samples
2016-05-17 | E-GEOD-77725 | biostudies-arrayexpress
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
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
Project description:Many innovative techniques and scientific improvements are available to tackle societal concerns, like public health safety and confining the risk of cancerous exposure to chemicals, but have not been thoroughly tested and implicated yet. We investigated if microRNA and mRNA transcription profiles can be implemented in a short-term carcinogen classifier assay. Our study is additionally focusing on the drawbacks of present-day carcinogen screening strategies and also aims to contribute to a more ethical approach towards animal use and welfare within risk assessment. Since current in vitro and in silico assays are still not able to mimic the in vivo situation accurately we set out to develop an alternative short-term in vivo assay. Five genotoxic, seven non-genotoxic and five non-carcinogen exposure studies were used to investigate if murine hepatic microRNA and mNA profiles after 7-day exposure are suitable tools to classify carcinogens. Classification analyses showed that a small transcript set, consisting of both microRNA and mRNA, is able to classify the genotoxic, non-genotoxic and non-carcinogens tested with 100% accuracy. The results indicate that microRNAs have the potential to be used as transcriptional classifiers and that a short-term transcriptional classifier assay in mice can be a powerful tool in carcinogenicity risk assessment. Since current in vitro and in silico assays are still not able to mimic the in vivo situation accurately we set out to develop an alternative short-term in vivo assay. Five genotoxic, seven non-genotoxic and five non-carcinogen exposure studies were used to investigate if murine hepatic microRNA and mNA profiles after 7-day exposure are suitable tools to classify carcinogens. Classification analyses showed that a small transcript set, consisting of both microRNA and mRNA, is able to classify the genotoxic, non-genotoxic and non-carcinogens tested with 100% accuracy. The results indicate that microRNAs have the potential to be used as transcriptional classifiers and that a short-term transcriptional classifier assay in mice can be a powerful tool in carcinogenicity risk assessment.
2014-04-01 | GSE43977 | GEO
Project description:Many innovative techniques and scientific improvements are available to tackle societal concerns, like public health safety and confining the risk of cancerous exposure to chemicals, but have not been thoroughly tested and implicated yet. We investigated if microRNA and mRNA transcription profiles can be implemented in a short-term carcinogen classifier assay. Our study is additionally focusing on the drawbacks of present-day carcinogen screening strategies and also aims to contribute to a more ethical approach towards animal use and welfare within risk assessment. Since current in vitro and in silico assays are still not able to mimic the in vivo situation accurately we set out to develop an alternative short-term in vivo assay. Five genotoxic, seven non-genotoxic and five non-carcinogen exposure studies were used to investigate if murine hepatic microRNA and mNA profiles after 7-day exposure are suitable tools to classify carcinogens. Classification analyses showed that a small transcript set, consisting of both microRNA and mRNA, is able to classify the genotoxic, non-genotoxic and non-carcinogens tested with 100% accuracy. The results indicate that microRNAs have the potential to be used as transcriptional classifiers and that a short-term transcriptional classifier assay in mice can be a powerful tool in carcinogenicity risk assessment. Since current in vitro and in silico assays are still not able to mimic the in vivo situation accurately we set out to develop an alternative short-term in vivo assay. Five genotoxic, seven non-genotoxic and five non-carcinogen exposure studies were used to investigate if murine hepatic microRNA and mNA profiles after 7-day exposure are suitable tools to classify carcinogens. Classification analyses showed that a small transcript set, consisting of both microRNA and mRNA, is able to classify the genotoxic, non-genotoxic and non-carcinogens tested with 100% accuracy. The results indicate that microRNAs have the potential to be used as transcriptional classifiers and that a short-term transcriptional classifier assay in mice can be a powerful tool in carcinogenicity risk assessment. [mRNA profling] 96 hepatic samples in total, 8 control untreated samples, replicates per treated group n=4-6
2014-04-01 | E-GEOD-43977 | biostudies-arrayexpress
Project description:Many innovative techniques and scientific improvements are available to tackle societal concerns, like public health safety and confining the risk of cancerous exposure to chemicals, but have not been thoroughly tested and implicated yet. We investigated if microRNA and mRNA transcription profiles can be implemented in a short-term carcinogen classifier assay. Our study is additionally focusing on the drawbacks of present-day carcinogen screening strategies and also aims to contribute to a more ethical approach towards animal use and welfare within risk assessment. Since current in vitro and in silico assays are still not able to mimic the in vivo situation accurately we set out to develop an alternative short-term in vivo assay. Five genotoxic, seven non-genotoxic and five non-carcinogen exposure studies were used to investigate if murine hepatic microRNA and mRNA profiles after 7-day exposure are suitable tools to classify carcinogens. Classification analyses showed that a small transcript set, consisting of both microRNA and mRNA, is able to classify the genotoxic, non-genotoxic and non-carcinogens tested with 100% accuracy. The results indicate that microRNAs have the potential to be used as transcriptional classifiers and that a short-term transcriptional classifier assay in mice can be a powerful tool in carcinogenicity risk assessment.
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