We propose comparing liver gene expression of WT and female ERKO mice early in the high-fat feeding period to animals fed a regular chow diet. Analyzing liver tissue before the fatty liver disease phenotype becomes severe will allow identification of target genes which may be causal.
Hormone signaling and fatty liver in females: analysis of estrogen receptor α mutant mice.
Sex, Specimen part
View SamplesThe cell of origin of hepatoblastoma in humans and mice (HB) is unknown; it has been hypothesized to be a transformed hepatocyte, an oval cell, or a multipotent hepatic progenitor cell. In mice, the current dogma is that HBs arise within hepatocellular neoplasms as a result of further transformation from a neoplastic hepatocyte. However, there is little evidence in the literature to support a direct relationship between these two cell types. Furthermore, due to differences in etiology and development of hepatoblastoma between mice and humans, many have questioned the relevance of these tumors in hazard identification and risk assessment. In order to better understand the relationship between hepatocellular carcinoma and hepatoblastoma, as well as better determine the molecular similarities between mouse and human hepatoblastoma, global gene expression analysis and targeted Hras and Ctnnb1 mutation analysis were performed using concurrent hepatoblastoma, hepatocellular carcinoma, and associated normal adjacent liver (in the context of vehicle control liver) samples from a recent National Toxicology Program chronic bioassay. The data from this study provides a better understanding of the origins of hepatoblastoma in the B6C3F1 mice and the relevance of mouse hepatoblastoma to humans when considering chemical exposures of potential human cancer risk.
Genomic Profiling Reveals Unique Molecular Alterations in Hepatoblastomas and Adjacent Hepatocellular Carcinomas in B6C3F1 Mice.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with polybrominated diphenyl ether 47 (PBDE47), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.0485, 0.485, 4.85, 48.5 or 485 mg/kg PBDE47, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with 1,3,5,7,9,11-hexabromocyclododecane (HBCD), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.06, 0.641, 6.41, 64.1 or 641 mg/kg HBCD, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with bis(2-ethylhexyl) tetrabromophthalate (TBPH), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.07, 0.71, 7.06, 70.6 or 706 mg/kg TBPH, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with tetrabromobisphenol A-bis(2,3-dibromopropyl ether) (TBBPA-DBPE), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.1, 0.94, 9.4, 94.3 or 943 mg/kg TBBPA.DBPE, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with hexachlorocyclopentadienyl-dibromocyclooctane (HCDBCO), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.05, 0.54, 5.41, 54.1 or 541 mg/kg HCDBCO, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with decabromodiphenyl oxide (decaBDE), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.1, 0.959, 9.59, 95.9 or 959 mg/kg decaBDE, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with decabromodiphenylethane (DBDPE), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.1, 0.97, 9.71, 97.1 or 970 mg/kg DBDPE, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View Samples