We have used primary MEFs derived from wild type and E2F4 null mice growing asynchrounously in serum to generate a signature for E2F4 pathway activation. 10 wild type and 10 E2F4 null samples were each assayed using the Affymetrics Mouse Genome 430A 2.0 array.
Patterns of cell signaling pathway activation that characterize mammary development.
No sample metadata fields
View SamplesEDI3 was shown to be relevant in cell migration, adhesion and spreading. Gene expression analysis was performed to determine the effect of EDI3 silencing in MCF7 cells in order to gain insight into potential underlying mechanisms.
EDI3 links choline metabolism to integrin expression, cell adhesion and spreading.
Specimen part, Cell line
View SamplesPlacentation differs in the BN rat strain when compared to HSD and DSS rat strains. Intrauterine trophoblast invasion is shallow and the junctional zone is underdeveloped in the BN rat. These structural differences are striking but their quantification is not conducive to high throughput analyses. In the rat, the junctional zone can be readily dissected and is more homogenous than other components of the placentation site. HSD and BN rat gestation day 18.5 junctional zone gene expression profiles were determined using DNA microarray analysis to identity placenta-associate quantitate traits.
Chromosome-substituted rat strains provide insights into the genetics of placentation.
Specimen part
View SamplesWe have made use of the E-myc transgenic mouse, a model for the study of B-cell lymphoma development that is initiated through a defined genetic alteration, to explore the contributions of additional somatic alterations that contribute to the heterogeneity of the resulting tumors. As one example of such heterogeneity, we have focused on the observation that lymphomas develop in E-myc mice with a variable time of onset. Twenty-five early-onset, 25 late-onset lymphomas and 10 normal samples were each assayed on an Affymetrix Mouse Genome 430 2.0 array.
Utilization of pathway signatures to reveal distinct types of B lymphoma in the Emicro-myc model and human diffuse large B-cell lymphoma.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Utilization of the Eμ-Myc mouse to model heterogeneity of therapeutic response.
Specimen part
View SamplesWe used gene expression data from E-myc mouse lymphomas to test various genomic signatures and select lymphomas for further study
Utilization of the Eμ-Myc mouse to model heterogeneity of therapeutic response.
Specimen part
View SamplesWe used gene expression data from E-myc mouse lymphomas to perform unsupervised analyses that identified two lymphoma subgroups.
Utilization of the Eμ-Myc mouse to model heterogeneity of therapeutic response.
Specimen part
View SamplesWe used gene expression data from E-myc mouse lymphomas to test various genomic signatures and select lymphomas for further study
Utilization of the Eμ-Myc mouse to model heterogeneity of therapeutic response.
Specimen part
View SamplesTest systems to identify developmental toxicants are urgently needed. A combination of human stem cell technology and transcriptome analysis was used here to provide proof-of-concept that toxicants with a related mode of action can be identified, and grouped for read-across. We chose a test system of developmental toxicity, related to the generation of neuroectoderm from pluripotent stem cells (UKN1), and exposed cells for six days to benchmark concentration (BMC) of histone deacetylase inhibitors (HDACi) valproic acid, trichostatin-A, vorinostat, belinostat, panobinostat and entinostat. To provide insight into their toxic action, we identified HDACi consensus genes, assigned them to superordinate biological processes, and mapped them to a human transcription factor network constructed from hundreds of transcriptome data sets. We also tested a heterogeneous group of mercurials (methylmercury, thimerosal, mercury(II)chloride, mercury(II)bromide, 4-chloromercuribenzoic acid, phenylmercuric acid) (BMCs). Microarray data were compared at the highest non-cytotoxic concentration for all 12 toxicants. A support vector machine (SVM)-based classifier predicted all HDACi correctly. For validation, the classifier was applied to legacy data sets of HDACi, and for each exposure situation, the SVM predictions correlated with the developmental toxicity. Finally, optimization of the classifier based on 100 probe sets showed that eight genes (F2RL2, TFAP2B, EDNRA, FOXD3, SIX3, MT1E, ETS1, LHX2) are sufficient to separate HDACi from mercurials. Our data demonstrate, how human stem cells and transcriptome analysis can be combined for mechanistic grouping and prediction of toxicants. Extension of this concept to mechanisms beyond HDACi would allow prediction of human developmental toxicity hazard of unknown compounds with the UKN1 test system.
A transcriptome-based classifier to identify developmental toxicants by stem cell testing: design, validation and optimization for histone deacetylase inhibitors.
Sex, Specimen part
View SamplesGPAM is well characterized in triglyceride synthesis, but has never been implicated in cancer. Our study report a role for GPAM in cell migration. Gene expression changes after GPAM silencing was investigated to gain insight into possible mechanisms underlying GPAM's role in cell migration.
Glycerol-3-phosphate Acyltransferase 1 Promotes Tumor Cell Migration and Poor Survival in Ovarian Carcinoma.
Specimen part, Cell line
View Samples