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accession-icon GSE68387
IMI MARCAR Project: towards novel biomarkers for cancer risk assessment
  • organism-icon Mus musculus, Rattus norvegicus, Homo sapiens
  • sample-icon 56 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Phenobarbital mediates an epigenetic switch at the constitutive androstane receptor (CAR) target gene Cyp2b10 in the liver of B6C3F1 mice.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment, Subject, Time

View Samples
accession-icon GSE34463
Phenobarbital mediates an epigenetic switch at the constitutive androstane receptor (CAR) target gene Cyp2b10 in the liver of B6C3F1 mice.
  • organism-icon Mus musculus
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Phenobarbital mediates an epigenetic switch at the constitutive androstane receptor (CAR) target gene Cyp2b10 in the liver of B6C3F1 mice.

Sample Metadata Fields

Sex, Specimen part, Treatment, Subject

View Samples
accession-icon GSE51358
Metabolic programs orchestrated by the activated Ha-ras and -catenin oncoproteins in mouse liver tumors
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE34423
Phenobarbital mediates an epigenetic switch at the constitutive androstane receptor (CAR) target gene Cyp2b10 in the liver of B6C3F1 mice [Expression array].
  • organism-icon Mus musculus
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon

Description

Evidence suggests that epigenetic perturbations are involved in the adverse effects associated with some drugs and toxicants, including certain classes of non-genotoxic carcinogens. Such epigenetic changes (altered DNA methylation and covalent histone modifications) may take place at the earliest stages of carcinogenesis and their identification holds great promise for biomedical research. Here, we evaluate the sensitivity and specificity of genome-wide epigenomic and transcriptomic profiling in phenobarbital (PB)-treated B6C3F1 mice, a well-characterized rodent model of non-genotoxic liver carcinogenesis. Methylated DNA Immunoprecipitation (MeDIP)-coupled microarray profiling of 17,967 promoter regions and 4,566 intergenic CpG islands was combined with genome-wide mRNA expression profiling to identify liver tissue-specific PB-mediated DNA methylation and transcriptional alterations. Only a limited number of significant anti-correlations were observed between PB-induced transcriptional and promoter-based DNA methylation perturbations. However, the constitutive androstane receptor (CAR) target gene Cyp2b10 was found to be concomitantly hypomethylated and transcriptionally activated in a liver tissue-specific manner following PB treatment. Furthermore, analysis of active and repressive histone modifications using chromatin immunoprecipitation revealed a strong PB-mediated epigenetic switch at the Cyp2b10 promoter. Our data reveal that PB-induced transcriptional perturbations are not generally associated with broad changes in the DNA methylation status at proximal promoters and suggest that the drug-inducible CAR pathway regulates an epigenetic switch from repressive to active chromatin at the target gene Cyp2b10. This study demonstrates the utility of integrated epigenomic and transcriptomic profiling for elucidating early mechanisms and biomarkers of non-genotoxic carcinogenesis.

Publication Title

Phenobarbital mediates an epigenetic switch at the constitutive androstane receptor (CAR) target gene Cyp2b10 in the liver of B6C3F1 mice.

Sample Metadata Fields

Sex, Specimen part, Treatment, Subject

View Samples
accession-icon GSE11415
C2C12 differentiation time course to observe changes between myoblasts and myotubes
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon

Description

This analysis compares various timepoints from Day -1, 50% confluency myoblasts to Day 5 post differentiation myotubes.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE51355
Metabolic programs orchestrated by the activated Ha-ras and -catenin oncoproteins in mouse liver tumors [mRNA]
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon

Description

The process of hepatocarcinogenesis in the diethylnitrosamine (DEN) initiation/phenobarbital (PB) promotion mouse model involves the selective clonal outgrowth of cells harboring oncogene mutations in Ha-ras, B-raf, or Ctnnb1. Here, we have characterized mouse liver tumors harboring either Ctnnb1 or Ha-ras mutations via integrated molecular profiling at the transcriptional and translational and post-translational levels. In addition, metabolites of the intermediary metabolism were quantified by high resultion 1H magic angle nuclear magnetic resonance (HR-MAS NMR). We have identified tumor characteristic genotype-specific differences in mRNA and miRNA expression, protein levels, and post-translational modifications and in metabolite levels that facilitate the molecular and biochemical stratification of tumor phenotypes. Bioinformatic integration of these data at the pathway level led to novel insights into tumor genotype-specific aberrant cell signaling and in particular to a better understanding of alterations in pathways of the cell intermediary metabolism, which are driven by the constitutive activation of the -Catenin and Ha-ras oncoproteins in tumors of the two genotypes.

Publication Title

Ha-ras and β-catenin oncoproteins orchestrate metabolic programs in mouse liver tumors.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE45577
Profiling of glycerol- and CTX-induced models of muscle regeneration in mice
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon

Description

Utilizing glycerol and cardiotoxin (CTX) injections in the tibialis anterior muscles of M. musculus provides models of skeletal muscle damages followed by skeletal muscle regeneration. In particular, glycerol-induced muscle regeneration is known to be associated with ectopic adipogenesis. We characterized genome-wide expression profiles of tibialis anterior muscles from wild-type mice injured by either glycerol or CTX injection. Our goal was to detect gene expression changes during the time course of glycerol-induced and CTX-induced muscle regeneration models, that can lead to ectopic adipocyte accumulation.

Publication Title

Genomic profiling reveals that transient adipogenic activation is a hallmark of mouse models of skeletal muscle regeneration.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE22007
Targeting resistance to Smoothened antagonists by inhibiting the PI3K pathway
  • organism-icon Mus musculus
  • sample-icon 42 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE22005
Medulloblastoma tumors derived from Ptch+/-HIC+/- transgenic mouse allografted in nude mice
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon

Description

Nude mice were allografted with medulloblastoma tumors derived from Ptch+/-HIC+/- transgenic mouse and treated with vehicle or NVP-LDE225.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE22006
Medulloblastoma tumors derived from Ptch+/-p53-/- transgenic mouse allografted in nude mice
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon

Description

Nude mice were allografted with medulloblastoma tumors derived from Ptch+/-p53-/- transgenic mouse and treated with vehicle or NVP-LDE225.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Treatment

View Samples

refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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