A collection of genetically engineered mouse models (GEMM) of colorectal cancer (CRC) were created, and primary tumors from these GEMMs were analyzed.
Cross-species analysis of genetically engineered mouse models of MAPK-driven colorectal cancer identifies hallmarks of the human disease.
Specimen part
View SamplesHeterotopic cardiac transplants were constructed in male Wistar Furth (allograft donor) and ACI (host) rats. Rats were divided into three groups consisting of no treatment, treatment with a sub-therapeutic dose of cyclosporin A, and treated with combination of a sub-therapeutic dose of cyclosporin A and allochimeric peptide. The allografts were harvested at defined periods post-transplantation and RNA was harvested to monitor gene expression changes resulting from the various treatments in T-cells and in heart cells.
Intragraft gene expression profile associated with the induction of tolerance by allochimeric MHC I in the rat heart transplantation model.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
BRAF V600E Mutant Colorectal Cancer Subtypes Based on Gene Expression.
Sex, Age, Subject
View SamplesSamples were taken from surgically resected tumor specimens from patients with colorectal cancer. The expression profiles were determined using the Affymetrix GeneChip Human Exon 1.0 ST Array version 2. Gene mutation status was determined using Sanger sequencing.
BRAF V600E Mutant Colorectal Cancer Subtypes Based on Gene Expression.
Sex, Age, Subject
View SamplesmRNA from 59 primary colorectal tumour samples were extracted and hybridized to HG-U133Plus 2.0 expression arrays. Mutation status for several genes were determined using Sanger sequencing.
BRAF V600E Mutant Colorectal Cancer Subtypes Based on Gene Expression.
Sex, Age, Subject
View SamplesWhe embryonic stem cells are in vitro expanded threir telomereres lengthen, in the absence of genetic manipulations, concomitant with the loss of heterochromatic marks. In order to analyze whether there would be changes in gene expression during in vitro expansion we performed RNA-seq and found no substantial differences in gene expression at passage 6 or 16. Overall design: Embryonic stem (ES) cells were derived from blastocysts expressing GFP in the Rosa26 locus. Four independent lines of ES were in vitro expanded to passage 16. Total RNA was extracted from each independent clones, RNA was extracted and prepared for RNA-seq.
Generation of mice with longer and better preserved telomeres in the absence of genetic manipulations.
Specimen part, Cell line, Treatment, Subject
View SamplesRecent studies suggest that telomerase promotes cell growth by mechanisms that extend beyond the rescue of critically short telomeres. The in vitro model of mTert overexpressing MEFs recapitulates fundamental aspects of the growth-promoting effects of mTert in vivo. First, in Terc-proficient cells, mTert overexpression favors escape from replicative senescence and enhances anchorage-independent growth in response to oncogenic stress, which fits well with previous data showing that mTert overexpression promotes tumor formation. Second, in Terc-deficient cells, retroviral transduction with mTert results in a delayed onset of immortalization and impairs colony formation in response to oncogenic stress, which is in agreement with the inhibitory effect of mTert overexpression on tumorigenesis in a Terc null mouse background. To unravel the molecular targets of telomerase that impact on cell growth, we compared the transcriptome of MEFs, before and after mTert introduction. We found that ectopic expression of mTert was associated with detectable gene expression changes (greater than 1.5-fold; validated by qRT-PCR) of 26 transcripts. Analysis of the observed transcriptional changes indicates that ectopic expression of mTert suppresses in a coordinated manner functionally related genes with overlapping roles in growth arrest, resistance to transformation, and apoptosis. We show that the majority of the telomerase target genes are growth-inhibitory, transforming growth factor-beta (TGF-beta) -inducible genes and provide functional evidence for the potential of telomerase to abrogate TGF-beta -mediated growth inhibition. Thus, in line with the current view that the diversity of TGF-beta responses is not so much a consequence of the use of different signaling pathways but caused by different ways of reading the output from the same basic pathway, we propose that the telomerase status of a cell creates a gene expression pattern that determines how cells read growth inhibitory signals, among them signals propagated through the TGF-beta pathway.
Expression of mTert in primary murine cells links the growth-promoting effects of telomerase to transforming growth factor-beta signaling.
No sample metadata fields
View SamplesThe PI3K/Akt signaling pathway impacts various aspects of CD8 T cell homeostasis, such as effect versus memory cell differentiation, during viral infection. We used microarrays to determine which downstream molecules were affected and what other signaling pathways were interconnected with the Akt pathway by constitutive activation of Akt in LCMV-infected CD8 T cells.
Signal integration by Akt regulates CD8 T cell effector and memory differentiation.
Sex, Specimen part, Treatment
View SamplesIn a transcriptome study of psoriatic (PP) vs. normal (NN) skin, we found a co-expressed gene module (N5) enriched 11.5-fold for lipid biosynthetic genes. We also observed fewer visible hairs in PP skin, compared to uninvolved (PN) or NN skin (p<0.0001). To ask whether these findings might be due to abnormalities of the pilosebaceous unit, we carried out 3D morphometric analysis of paired PP and PN biopsies. Sebaceous glands (SG) were markedly atrophic in PP vs. PN skin (91% average reduction in volume, p=0.031). Module N5 genes were strongly downregulated in PP vs. NN skin (fold-change [FC] < 0.25, 44.4-fold), and strongly up-regulated in sebaceous hyperplasia (SH, FC > 4, 54.1-fold). The intersection of PP-downregulated and SH-upregulated gene lists generated a gene expression signature consisting solely of module N5 genes, whose expression in PP vs. NN skin was inversely correlated with the signature of IL17-stimuated keratinocytes. Despite loss of visible hairs, morphometry identified elongated follicles in PP vs. PN skin (average 1.7 vs. 1.2 Jm, p=0.020). These results document SG atrophy in non-scalp psoriasis, identify a cytokine-regulated set of SG signature genes, and suggest that loss of visible hair in PP skin may result from abnormal SG function.
Sebaceous Gland Atrophy in Psoriasis: An Explanation for Psoriatic Alopecia?
Specimen part, Disease, Disease stage
View SamplesLineage commitment during Embryonic Stem Cells (ESCs) differentiation is controlled not only by a gamut of transcription factors but also by epigenetic events, mainly histone deacetylation and promoter DNA methylation. Moreover, the DNA demethylation agent 5-Aza-2-deoxycytidine (AzadC) has been widely described in the literature as an effective chemical stimulus used to promote cardiomyogenic differentiation in various stem cell types; however, its toxicity and instability complicate its use. Thus, the purpose of this study was to examine the effects of zebularine, a stable and non-toxic DNA cytosine methylation inhibitor, on ESCs differentiation. Herein are the Affymetrix Expression data obtained from RNA of murine ESCs treated with zebularine.
Zebularine regulates early stages of mESC differentiation: effect on cardiac commitment.
Specimen part, Cell line, Treatment
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