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Homo sapiens
12 Downloadable Samples
Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
MicroRNA and transcriptome analysis in periocular Sebaceous Gland Carcinoma.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
Samples were taken from patients undergoing cancer excision for pagetoid (wide) sebaceous gland carcinoma (SGC) and different individuals undergoing excision for nodular (local) SGC.
Publication Title
MicroRNA and transcriptome analysis in periocular Sebaceous Gland Carcinoma.
Sample Metadata Fields
Specimen part
View Samples- Zea mays
- 12 Downloadable Samples
Illumina Genome Analyzer IIx, Illumina HiSeq 2000, Illumina Genome Analyzer
Description
Small RNAs (sRNAs) are hypothesized to contribute to hybrid vigor because they maintain genome integrity, contribute to genetic diversity, and control gene expression. We used Illumina sequencing to assess how sRNA populations vary between two maize inbred lines (B73, Mo17) and their hybrid. We sampled sRNAs from the seedling shoot apex and the developing ear, two rapidly growing tissues that program the greater growth of maize hybrids. We found that parental differences in siRNAs primarily originate from repeat regions. Although the maize genome contains greater number and complexity of repeats compared to Arabidopsis or rice, we confirmed that like these simpler plant genomes, 24-nt siRNAs whose abundance differs between maize parents also show a trend of downregulation following hybridization. Surprisingly, hybrid vigor is fully maintained when 24-nt siRNAs are globally reduced by mutation of the RNA-dependent RNA polymerase2 (RDR2) encoded by modifier of paramutation1 (mop1). We also discovered that 21-22nt siRNAs derived from a number of distinct retrotransposon families differentially accumulate between B73 and Mo17 as well as their hybrid. Thus, maize possesses a novel source of genetic variation for regulating both transposons and genes at a genomic scale, which may contribute to its high degree of observed heterosis. Overall design: sRNA libraries were derived from RNA isolated from the seedling shoot apex and developing ear tissues from B73, Mo17, B73xMo17 and Mo17xB73. The shoot apex was chosen because it is enriched for meristematic tissue where cell proliferation occurs, rates of organ initiation are determined, and organ size is specified. The developing ear was examined because it is enriched in meristematic tissue and is undergoing rapid growth, and also because the mature ear shows the highest degree of heterosis. Total RNA was isolated and separated on a 15% TBE-Urea polyacrylamide gel. Using a 10-bp ladder, the sRNA fraction representing 10-40-bp was excised. sRNA libraries were prepared according to Lu et al. (2007) or manufacturer''s instructitions (Illumina). A combination of Perl scripts and FASTX toolkit scripts were used to remove adapters, collapse identical sequences and count reads per sequence. Supplementary processed data text files contain the distinct sRNA sequences for all of the genotypes analyzed in that experiment. Abundance (reads per million) was calculated for each distinct sequence by dividing the number of reads of distinct sRNA in a library by the total number of sRNA reads for that library and multiplying this by 1 million. Genome builds: B73 genome, maizesequence.org release 4a.53 (October, 2009); Mo17 whole genome shotgun clones.
Publication Title
Repeat associated small RNAs vary among parents and following hybridization in maize.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 19 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302), Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Atherosclerosis is a transmural chronic inflammatory condition of small and large arteries that is associated with adaptive immune responses at all disease stages. However, impacts of adaptive immune reactions on clinically apparent atherosclerosis such as intima lesion (plaque) rupture, thrombosis, myocardial infarction, and aneurysm largely remain to be identified. It is increasingly recognized that leukocyte infiltrates in plaque, media, and adventitia are distinct but their specific roles have not been defined. To map these infiltrates, we employed laser capture microdissection (LCM) to isolate the three arterial wall laminae using apoE-/- mouse aorta as a model. RNA from LCM-separated tissues was extracted and large scale whole genome expression microarrays were prepared. We observed that the quality of the resulting gene expression maps was compromised by tissue RNA carried over from adjacent laminae during LCM. To account for these flaws, we established quality controls and algorithms to improve the predictive power of LCM-derived microarray data. Our approach creates robust transcriptome atlases of normal and atherosclerotic aorta. Assessing LCM transcriptomes for immunity-related mRNAs indicated markedly distinctive gene expression patterns in the three laminae of the atherosclerotic aorta. These mouse mRNA expression data banks can now be mined to address a wide range of questions in cardiovascular biology.
Publication Title
The lamina adventitia is the major site of immune cell accumulation in standard chow-fed apolipoprotein E-deficient mice.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 24 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
High-density lipoproteins (HDLs) protect pancreatic cells against apoptosis. This property might be related to the increased risk to develop diabetes in patients with low HDL blood levels. However, the mechanisms by which HDLs protect cells are poorly characterized. Here we use a transcriptomic approach to identify genes differentially modulated by HDLs in cells subjected to apoptotic stimuli.
Publication Title
Involvement of 4E-BP1 in the protection induced by HDLs on pancreatic beta-cells.
Sample Metadata Fields
Specimen part, Cell line
View Samples
SRP084282- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
Hepatocellular carcinoma (HCC) represents the fifth most common form of cancer worldwide and carries a high mortality rate due to lack of effective treatment. Males are eight times more likely to develop HCC that females, an effect largely driven by sex hormones, albeit through still poorly understood mechanisms. We previously identified TRIM28, a scaffold protein capable of recruiting a number of chromatin modifiers, as a crucial mediator of sexual dimorphism in the liver, with Trim28hep-/- mice displaying sex-specific transcriptional deregulation of a wide range of bile and steroid metabolism genes and development of liver adenomas in males. We now demonstrate that obesity and ageing precipitate alterations of TRIM28-dependent transcriptional dynamics, leading to a metabolic infection state responsible for highly penetrant male-restricted hepatic carcinogenesis. Molecular analyses implicate aberrant androgen receptor stimulation, biliary acid disturbances and altered responses to gut microbiota in the pathogenesis of Trim28hep-/--associated HCC. Correspondingly, androgen deprivation markedly attenuates the frequency and severity of tumors, and raising animals under axenic conditions completely abrogates their abnormal phenotype, even upon high-fat diet challenge. This work underpins how discrete polyphenic traits in epigenetically unstable conditions can contribute to a cancer-prone state, and more broadly provides new evidence linking hormonal imbalances, metabolic disturbances, gut microbiota and cancer. Overall design: Transcriptome profiling of liver tissues from TgAlbCre or TgAlbCreKap1lox mice in HFD settings
Publication Title
Polyphenic trait promotes liver cancer in a model of epigenetic instability in mice.
Sample Metadata Fields
Specimen part, Subject, Time
View Samples- Homo sapiens
- 320 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [HuEx-1_0-st-v2.hg18.custom ENTREZG (huex10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Integrative analyses reveal signaling pathways underlying familial breast cancer susceptibility.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 160 Downloadable Samples
Affymetrix Human Exon 1.0 ST Array [HuEx-1_0-st-v2.hg18.custom ENTREZG (huex10st)
Description
We obtained peripheral blood samples for women from Utah (USA) and Ontario (Canada) who had a family history of breast cancer (or did not), who carried a BRCA1/2 mutation (or did not), and who had developed breast cancer (or had not).
Publication Title
Integrative analyses reveal signaling pathways underlying familial breast cancer susceptibility.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 160 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [HuEx-1_0-st-v2.hg18.custom ENTREZG (huex10st)
Description
We obtained peripheral blood samples for women from Utah (USA) and Ontario (Canada) who had a family history of breast cancer (or did not), who carried a BRCA1/2 mutation (or did not), and who had developed breast cancer (or had not).
Publication Title
Integrative analyses reveal signaling pathways underlying familial breast cancer susceptibility.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 24 Downloadable Samples
- Illumina HiSeq 2500
Description
Canonical Wnt signaling output is mediated by ß-catenin, which interacts with LEF/TCF transcription factors and recruits a general transcriptional activation complex to its C-terminus. Its N-terminus binds BCL9/9L proteins, which bind co-activators that in mammals contribute to fine-tuning the transcriptional output. We found that a BCL9/9L-dependent gene expression signature was strongly associated with patient outcome in colorectal cancer and that stem cell and mesenchymal genes determine its prognostic value. Abrogating BCL9/9L-ß-catenin signaling in independent mouse colorectal cancer models resulted in virtual loss of these traits, and oncogenic intestinal organoids lacking BCL9/9L proteins proved no longer tumorigenic. Our findings suggest that the BCL9/9L arm of Wnt-ß-catenin signaling sustains a stemness-to-differentiation equilibrium in colorectal cancer, which critically affects disease outcome. Mutational activation of the Wnt pathway is a key oncogenic event in colorectal cancer. Targeting the pathway downstream of activating mutations is challenging, and the therapeutic window is limited by intestinal toxicity. Contrasting with phenotypes caused by inactivating key Wnt pathway components, ablation of BCL9/9L proteins in adult mice indicated that they were dispensable for intestinal homeostasis, consistent with their role in tuning transcription. Cancer stem cells are increasingly recognized as responsible for tumor recurrence. The correlation between stemness traits in colorectal cancer models and BCL9/9L-ß-catenin signaling suggests that high Wnt signaling output is required for their maintenance. Our findings suggest that pruning Wnt-ß-catenin signaling might be well tolerated and prove sufficient for trimming stemness traits and improving disease outcome. Overall design: Examination of Bcl9/9l-knockout versus wild-type transcriptome in murine AOM-DSS tumors, APC-Kras tumors and healthy colocyte extracts.
Publication Title
BCL9/9L-β-catenin Signaling is Associated With Poor Outcome in Colorectal Cancer.
Sample Metadata Fields
No sample metadata fields
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