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GSE58812
Homo sapiens
98 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Triple-negative (TN) breast cancers need to be refined in order to identify therapeutic subgroups of patients.
Publication Title
Gene-expression molecular subtyping of triple-negative breast cancer tumours: importance of immune response.
Sample Metadata Fields
Disease
View Samples- Homo sapiens
- 602 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Innovative approaches combining regulatory networks and genomic data are needed to extract pertinent biological informations to a better understanding of complex disease such as cancer and improve identi cation of entities leading to potential new therapeutic avenues. In this study, we confronted an automatic generated regulatory network with gene expression pro les (GEP) from a large cohort of patients with multiple myeloma (MM) and normal individuals with a causality reasonning method based of graph coloring to identify keynodes. Due to this causality reasoning, it is possible to infer proteins state from these GEP. Also, our method is able to simulate the impact of the perturbation of a node in this regulatory network to identify therapeutic targets. This method allowed us to nd that JUN/FOS and FOXM1, known in MM, and their inhibition as speci c to large group of patients with MM. Moreover, we associated the inhibition of FOXM1 activity with good prognosis, suggesting the inhibition of FOXM1 activity could be a survival marker. Finally, if JUN/FOS activation seems to be a way to strongly perturb the regulatory network in view of GEP, our result suggests the activation of FOXM1 could be interesting way to perturb some sub-group of profiles.
Publication Title
Logic programming reveals alteration of key transcription factors in multiple myeloma.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Mus musculus
- 16 Downloadable Samples
Illumina HiSeq 1500
Description
PEST-domain-enriched tyrosine phosphatase (PEP) is a cytoplasmic protein tyrosine phosphatase that regulates immune cell functions, including mast cell functions. Using bone marrow derived mast cells (BMMCs) from PEP+/+ and PEP-/- mice, RNA-seq data showed that dinitrophenol (DNP) - activated PEP-/- BMMCs have misregulated gene expression, with some cytokine/chemokine genes (eg.TNFa, IL13, CSF2) showing reduced gene expression in the dinitrophenol (DNP) - activated PEP-/- BMMCs compared to (DNP)-activated PEP+/+ BMMCs. Also, the ability of the glucocorticoid dexamethasone (Dex) to negatively regulate DNP - induced COX-2 gene expression in PEP-/- BMMCs was inhibited compared to the PEP+/+ BMMCs. Overall design: Biological replicates are sequenced and analyzed. The samples are either wild-type or mutant for PEP and cells were sensitized with Ig-E, activated with Dinitrophenol and glucocorticoid treatment done with Dexamethasone.
Publication Title
Transcriptomic data on the role of PEST-domain-enriched tyrosine phosphatase in the regulation of antigen-mediated activation and antiallergic action of glucocorticoids in mast cells.
Sample Metadata Fields
Sex, Specimen part, Cell line, Treatment, Subject
View Samples- Homo sapiens
- 23 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st), Affymetrix Mapping 250K Nsp SNP Array (mapping250knsp)
Description
In this study we addressed subclonal evolutionary process after treatment and subsequent relapse in multiple myeloma (MM) in a cohort of 24 MM patients treated either with conventional chemotherapy or with the proteasome inhibitor, bortezomib. Because MM is a highly heterogeneous disease coupled with a large number of DNA copy number alterations (CNAs) and loss of heterozygosity (LOH), we focused our study on the secondary genetic events: 1q21 gain, NF-kB activating mutations, RB1 and TP53 deletions, that seem to reflect progression. By using genome-wide high resolution SNP arrays we identified subclones with nonlinear complex evolutionary histories in a third of patients with myeloma, the relapse clone apparently derived from a minor subclone at diagnosis. Such reordering of the spectrum of genetic lesions during therapy is likely to reflect selection of genetically distinct subclones not initially competitive against the dominant population that survived chemotherapy, thrived and acquired new anomalies. In addition we found that emergence of minor subclones at relapse was significantly associated with bortezomib treatment. Altogether, these data support the idea of new strategy of future clinical trials in MM that would combine targeted therapy and subpopulations control to eradicate all myeloma subclones in order to obtain long-term remission.
Publication Title
Minor clone provides a reservoir for relapse in multiple myeloma.
Sample Metadata Fields
Specimen part, Disease, Cell line, Subject
View Samples- Homo sapiens
- 23 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Series GSE25262 patients on expression side.
Publication Title
Minor clone provides a reservoir for relapse in multiple myeloma.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 34 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Human induced pluripotent stem cells as a tool to model a form of Leber congenital amaurosis.
Sample Metadata Fields
Sex, Specimen part, Cell line
View Samples- Homo sapiens
- 21 Downloadable Samples
Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Our purpose was to investigate genes and molecular mechanisms involved in patients with Leber congenital amaurosis (LCA). Fibroblasts from two unrelated clinically-identified patients (Coriell) were reprogrammed to pluripotency by retroviral transduction. These human induced Pluripotent Stem Cells (hiPSCs) were differentiated into neural stem cells (NSC) that mimicked the neural tube stage and retinal pigmented epithelial (RPE) cells that could be targeted by the disease. A genome wide transcriptome analysis was performed with Affymetrix Exon Array GeneChip, comparing LCA-hiPSCs derivatives to controls. The aim was to identify differentially expressed genes which may be associated with early developmental defect before the establishment of mature retinal circuitry.
Publication Title
Human induced pluripotent stem cells as a tool to model a form of Leber congenital amaurosis.
Sample Metadata Fields
Sex, Specimen part, Cell line
View Samples- Homo sapiens
- 13 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Our purpose was to investigate genes and molecular mechanisms involved in patients with Leber congenital amaurosis (LCA). Fibroblasts from two unrelated clinically-identified patients (Coriell) were reprogrammed to pluripotency by retroviral transduction. These human induced Pluripotent Stem Cells (hiPSCs) were differentiated into neural stem cells (NSC) that mimicked the neural tube stage and retinal pigmented epithelial (RPE) cells that could be targeted by the disease. A genome wide transcriptome analysis was performed with Affymetrix Exon Array GeneChip, comparing LCA-hiPSCs derivatives to controls. The aim was to identify differentially expressed genes which may be associated with early developmental defect before the establishment of mature retinal circuitry.
Publication Title
Human induced pluripotent stem cells as a tool to model a form of Leber congenital amaurosis.
Sample Metadata Fields
Sex, Specimen part, Cell line
View Samples- Saccharomyces cerevisiae
- 8 Downloadable Samples
- Affymetrix Yeast Genome 2.0 Array (yeast2)
Description
This data provides evidence that elevation of cAMP levels has a dramatic effect on the transcriptome of yeast cells, with particular emphasis on mitochondrial function and the promotion of ROS production
Publication Title
cAMP/PKA signaling balances respiratory activity with mitochondria dependent apoptosis via transcriptional regulation.
Sample Metadata Fields
Treatment
View Samples- Danio rerio
- 6 Downloadable Samples
- IlluminaHiSeq1500
Description
Somatic mutations activating MAPK signaling in disorders of brain overgrowth and in diffuse glioma have recently been reported in pediatric neurology. Here we developed a progressive zebrafish model of glioma based on somatic expression of oncogenes that activate MAPK-AKT signalling (H-RASG12V, K-RASG12D, AKT, EGFRv3, BRAFV600E) in neural progenitor cells. Oncogenic HRAS was the most effective in activating MAPK signaling and caused the development of different types of growth disorders in juvenile fish: from benign dysplasia/heterotopia to invasive tumors of the telencephalon, midbrain and cerebellum. We used this model to clarify the molecular events leading to malignant tumors instead of benign lesions. Specific signatures distinguish benign heterotopia from tumors and establish that tumors require persistent activation of MAPK/ERK. Moreover, analysis of global RNA expression showed that brain tumors expressed a gene signature similar to the mesenchymal glioblastoma subtype Overall design: We performed transcriptome analysis (RNA-Seq) of 3 UAS:HRASV12G brains, which carried tumorigenic lesions in the telencephalon, midbrain and IV ventricle and compared them with tumor free, age matched brains.
Publication Title
A novel brain tumour model in zebrafish reveals the role of YAP activation in MAPK- and PI3K-induced malignant growth.
Sample Metadata Fields
No sample metadata fields
View Samples