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GSE35495
Mus musculus, Homo sapiens
42 Downloadable Samples
Affymetrix Human Genome U133A Array (hgu133a), Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Genetic programs expressed in resting and IL-4 alternatively activated mouse and human macrophages: similarities and differences.
Sample Metadata Fields
Specimen part, Disease, Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Analysis of alternative activation of macrophages at gene expression level. The study forms part of a wider study where we compare the effects of IL-4 in different human and mouse macrophages. Our results support the notion that in vitro culture conditions greatly affect the macrophage response to IL-4.
Publication Title
Genetic programs expressed in resting and IL-4 alternatively activated mouse and human macrophages: similarities and differences.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302), Affymetrix Human Genome U133A Array (hgu133a)
Description
Analysis of alternative activation of macrophages at gene expression level. The study forms part of a wider study where we compare the effects of IL-4 in different human and mouse macrophages. Our results support the notion that in vitro culture conditions greatly affect the macrophage response to IL-4.
Publication Title
Genetic programs expressed in resting and IL-4 alternatively activated mouse and human macrophages: similarities and differences.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 9 Downloadable Samples
NextSeq500
Description
We used parkin –overexpressing MRC5 fibroblasts to investigate the role of mitochondria deficiency on senescence-associated gene expression. Overall design: RNA-seq analysis on proliferating and senescent Parkin-expressing MRC5 fibroblasts treated with CCCP (treated) or DMSO (Untreated).
Publication Title
Mitochondria are required for pro-ageing features of the senescent phenotype.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 36 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Background: Acute myeloid leukemia (AML) is driven by somatic mutations and genomic rearrangements affecting >20 genes. Many of these are recent discoveries and how this molecular heterogeneity dictates AML pathophysiology and clinical outcome remains unclear. Methods: We sequenced 111 leukemia genes for driver mutations in 1540 AML patients with cytogenetic and clinical data. We modeled AMLs genomic structure, defining genetic interactions, patterns of temporal evolution and clinical correlations. Results: We identified 5,236 driver mutations involving 77 loci, including hotspot mutations in MYC. We found 1 driver mutation in 96% patients, and 2 in 85%. Gene mutations implicated in age related clonal hematopoiesis (DNMT3A, ASXL1, TET2) were the earliest in AML evolution, followed by highly specific and ordered patterns of co-mutation in chromatin, transcription and splicing regulators, NPM1 and signaling genes. The patterns of co-mutation compartmentalize AML into 12 discrete molecular classes, each presenting with distinct clinical manifestation. Amongst these, mutations in chromatin and spliceosome genes demarcate a molecularly heterogeneous subgroup enriched for older AML patients currently classified as intermediate risk and results in adverse prognosis. Two- and three-way genetic interactions often implicating rare genes/mutation-hotspots, markedly redefined clinical response and long-term curability, with the NPM1:DNMT3A:FLT3ITD genotype (6% patients) identifying poor prognosis disease, whereas within the same class NPM1:DNMT3A:NRASG12/13 (3%) associated with favorable outlooks. Conclusions: 79% of AML is molecularly classified in 12 genomic subgroups. These represent distinct molecular phylogenies, implicating complex genotypes. Delineation of higher-order genomic relationships, guide the development of personally tailored classification, prognostication and clinical protocols. Similar studies across cancer types are warranted.
Publication Title
Genomic Classification and Prognosis in Acute Myeloid Leukemia.
Sample Metadata Fields
Specimen part, Disease
View Samples- Mus musculus
- 10 Downloadable Samples
- NextSeq 500
Description
Ageing is the biggest risk factor to cardiovascular health and is associated with increased incidence of cardiovascular disease. Cellular senescence, a process driven in part by telomere shortening has been implicated in age-related cardiac dysfunction. However, the role of cellular senescence and its underlying mechanisms in slowly dividing/post-mitotic cardiomyocytes is not understood. Overall design: We quantify transcription via high throughput RNA sequencing in young (3 months) and old (20 months) mouse cardiomyocytes.
Publication Title
Length-independent telomere damage drives post-mitotic cardiomyocyte senescence.
Sample Metadata Fields
Age, Cell line, Subject
View Samples- Mus musculus
- 15 Downloadable Samples
- Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
We tamoxifen treated 8-12 week old mice that had floxed alleles of the following: 1) both Apc alleles (giving rise to Apc truncation/inactivation); 2) both Cdx2 alleles (giving rise to Cdx2 inactivation; 3) one Braf allele, that upon Cre-mediated recombination gives a Braf V600E mutant allele (details below), and 4) the combination of both the Cdx2 alleles and the BrafV600E allele. All four of those groups also had a CDX2P-CreERT2 transgene that expresses Cre recombinase fused to a tamoxifen-regulated fragment of the estrogen receptor ligand binding domain. CreERT2 expression occurs only in tissues where the Cdx2 gene is expressed, which is almost exclusively in adult mouse cecum and colon epithelium. A fifth group of mice had the floxed Cdx2 alleles, but no CDX2P-CreERT2 gene. Treating the mice having CDX2P-CreERT2 with tamoxifen permits the Cre recombinase to enter the cell nucleus and recombine the Apc, Braf, and/or Cdx2 alleles containing loxP sequence elements. Mice were treated with intraperitoneal injection of tamoxifen dissolved in corn oil. Three mice per group were used. The control mice did not develop tumors or any morphological or histological changes in their epithelium, but their colons were used to create the 3 control samples. To obtain the BrafV600E allele we used a genetically engineered mouse line previously described by Dankort et al. (Genes Dev 2007, 21:379-84) that can express the BrafV600E mutant protein following Cre-mediated recombination. The Braf(CA) (Braf-Cre-activated) allele mice carry a gene-targeted allele of Braf, where Braf sequences from exons 15-18 are present in the normal mouse Braf intron 14, followed by a mutated exon 15 (carrying the V600E mutation). The exon 15-18 sequence element is flanked by loxP sites. In the absence of Cre-mediated recombination, the Braf(CA) allele expresses a wild type Braf protein. Following Cre-mediated recombination, the Braf exon 15-18 element is removed, and the Braf(CA) allele then encodes the Braf V600E protein (from the introduced mutated exon 15). RNA was purified from tumor or normal tissue, and targets for Affymetrix arrays were synthesized from the mRNAs. We used Affymetrix Mouse Gene 2.1 ST arrays, which hold 41345 probe-sets, but we largely analyzed just those 25216 probe-sets that were mapped to Entrez gene IDs. Raw data was processed with the Robust Multi-array Average algorithm (RMA). Data is log2-transformed transcript abundance estimates. We fit a one-way ANOVA model to the five groups of samples. We supply a supplementary excel workbook that holds the same data as the data matrix file, but also holds the probe-set annotation at the time we analyzed the data, and some simple statistical calculations, which selects subsets of the probe-sets as differentially expressed between pairs of groups, as well as significant Cdx2-/- by Braf V600E interactions. It also gives the homologous human gene IDs we used for enrichment testing, which were 1-to-1 best homologs according to build 68 of NCBI's Homologene. A second supplementary sheet shows the data we enrichment tested after collapsing to distinct human homologs, joins of the results of tests with GSE4045 data and of tests with TCGA data to the mouse genes, and the intersections of selected genes in those data set with our gene selections in mouse. Consumers should consider obtaining more up-to-date probe-set annotation for the array platform.
Publication Title
BRAF<sup>V600E</sup> cooperates with CDX2 inactivation to promote serrated colorectal tumorigenesis.
Sample Metadata Fields
Sex, Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HiSeq 2500
Description
To study the host transcriptome of human fibroblasts after infection with T. gondii (Type I-RH). Overall design: Three bioloigcal replicates of uninfected HFFs and three biological replicates of T. gondii (Type I-RH) infected HFFs were sequenced using directional RNA-seq.
Publication Title
SMITE: an R/Bioconductor package that identifies network modules by integrating genomic and epigenomic information.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 41 Downloadable Samples
- Illumina HiSeq 2500
Description
We compare the CD4+ T cell transcriptome between obese and normal-weight children with asthma to identify molecules/pathways differentially expressed in obese asthmatic CD4+ T cells Overall design: CD4+ T cell transcriptome generated using Directional RNA-Seq library preparatio; A=Normal-weight, B=obese
Publication Title
CDC42-related genes are upregulated in helper T cells from obese asthmatic children.
Sample Metadata Fields
Sex, Age, Specimen part, Disease stage, Race, Subject
View Samples- Homo sapiens
- 67 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We performed DNA methylation (HELP array) and gene expression profiling in 69 samples of diffuse large B cell lymphoma (DLBCL). First, by gene expression, two molecular subtypes of DLBCL termed as "germinal center B cell-like" (GCB) and "activated B cell-like" (ABC) DLBCL were assigned to the 69 DLBCL cases. Then, the supervised analysis using HELP data revealed strikingly different DNA promoter methylation patterns in the two molecular DLBCL subtypes. These data provide epigenetic evidence that the DLBCL subtypes are distinct diseases that utilize different oncogenic pathways.
Publication Title
DNA methylation signatures define molecular subtypes of diffuse large B-cell lymphoma.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples