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GSE59949
Homo sapiens
4 Downloadable Samples
Affymetrix Human Gene 1.1 ST Array (hugene11st)
Description
We analysed the genexpression of dental follicle cells (DFCs) after 3 days osteogenic differentiation with BMP2 after transfection with a DLX3 plasmid (pDLX3) and after transfection with an empty plasmid (pEV)
Publication Title
A protein kinase A (PKA)/β-catenin pathway sustains the BMP2/DLX3-induced osteogenic differentiation in dental follicle cells (DFCs).
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 26 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The goal of the experiment: To characterize the dynamic gene expression profile of engineered human skin in vitro and after grafting, and compare with expression profile of uninjured human skin.
Publication Title
Engineered human skin substitutes undergo large-scale genomic reprogramming and normal skin-like maturation after transplantation to athymic mice.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
MCF7 and BT474 cell lines were exposed to LTED culture for 0 and 2 days, 6 weeks and 10 months and monitored for changes in gene expression
Publication Title
Clinical instability of breast cancer markers is reflected in long-term in vitro estrogen deprivation studies.
Sample Metadata Fields
Cell line, Treatment, Time
View Samples- Homo sapiens
- 41 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
An immediate-late gene expression module decodes ERK signal duration.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 41 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
We integrate experimental data and mathematical modelling to unveil how ERK signal duration is relayed to mRNA dynamics.
Publication Title
An immediate-late gene expression module decodes ERK signal duration.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 24 Downloadable Samples
- Affymetrix Human Gene 2.1 ST Array (hugene21st)
Description
The oncogenic mechanisms and tumour biology underpinning Clear Cell Sarcoma of Kidney (CCSK), the second commonest paediatric renal malignancy, are poorly understood and currently therapy depends heavily on Doxorubicin with cardiotoxic side-effects. Previously, we characterised the balanced t(10;17)(q22;p13) chromosomal translocation, identified at that time as the only recurrent genetic aberration in CCSK. This translocation results in an in-frame fusion of the YWHAE (encoding 14-3-3e) and NUTM2 genes, with a somatic incidence of 12%. Clinico-pathological features of that cohort suggested that this aberration might be associated with higher stage and grade disease. Since no primary CCSK cell line exists, we generated various stably transfected cell lines containing doxycycline-inducible HA-tagged-YWHAE-NUTM2, in order to study the effect of expressing this transcript. 14-3-3e-NUTM2-expressing cells exhibited significantly greater cell migration compared to mock-treated controls. Gene and protein expression studies conducted in parallel on this model system suggested dysregulation of signalling pathways as a basis to the migration changes. Importantly, by blocking these signalling pathways using anti-EGFR, anti-IGF1R and anti-PDGFa neutralising antibodies, the migratory advantage conferred by transcript expression was abrogated. These results support 14-3-3e-NUTM2 expression as a contributor to CCSK tumorigenesis and provide avenues for the exploration of novel therapeutic approaches in CCSK.
Publication Title
Dysregulated mitogen-activated protein kinase signalling as an oncogenic basis for clear cell sarcoma of the kidney.
Sample Metadata Fields
Disease, Cell line
View Samples- Homo sapiens
- 24 Downloadable Samples
Illumina HiSeq 2000
Description
Aberrant cell signaling can cause cancer and other diseases and is a focal point of drug research. A common approach is to infer signaling activity of pathways from gene expression. However, mapping gene expression to pathway components disregards the effect of post-translational modifications, and downstream signatures represent very specific experimental conditions. Here we present PROGENy, a method that overcomes both limitations by leveraging a large compendium of publicly available perturbation experiments to yield a common core of Pathway RespOnsive GENes. Unlike existing methods, PROGENy can (i) recover the effect of known driver mutations, (ii) provide or improve strong markers for drug indications, and (iii) distinguish between oncogenic and tumor suppressor pathways for patient survival. Collectively, these results show that PROGENy accurately infers pathway activity from gene expression. Overall design: HEK293?RAF1:ER cells were treated with different stimuli (4OHT, Ly29002, TNFa, TGF1b, IFNg) for different periods of time (1h, 4h).
Publication Title
Perturbation-response genes reveal signaling footprints in cancer gene expression.
Sample Metadata Fields
Specimen part, Subject
View Samples- Rattus norvegicus
- 18 Downloadable Samples
- Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Reverse engineering a hierarchical regulatory network downstream of oncogenic KRAS.
Sample Metadata Fields
Cell line, Treatment
View Samples- Rattus norvegicus
- 16 Downloadable Samples
- Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
RAS mutations are highly relevant for progression and therapy response of human tumours, but the genetic network that ultimately executes the oncogenic effects is poorly understood. Here we used a reverse-engineering approach in an ovarian cancer model to reconstruct KRAS oncogene-dependent cytoplasmic and transcriptional networks from perturbation experiments based on gene silencing and pathway inhibitor treatments. We measured mRNA and protein levels in manipulated cells by microarray, RT-PCR and Western Blot analysis, respectively. The reconstructed model revealed complex interactions among the transcriptional and cytoplasmic components, some of which were confirmed by double pertubation experiments. Interestingly, the transcription factors decomposed into two hierarchically arranged groups. To validate the model predictions we analysed growth parameters and transcriptional deregulation in the KRAS-transformed epithelial cells. As predicted by the model, we found two functional groups among the selected transcription factors. The experiments thus confirmed the predicted hierarchical transcription factor regulation and showed that the hierarchy manifests itself in downstream gene expression patterns and phenotype.
Publication Title
Reverse engineering a hierarchical regulatory network downstream of oncogenic KRAS.
Sample Metadata Fields
Cell line, Treatment
View Samples- Rattus norvegicus
- 2 Downloadable Samples
Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
RAS mutations are highly relevant for progression and therapy response of human tumours, but the genetic network that ultimately executes the oncogenic effects is poorly understood. Here we used a reverse-engineering approach in an ovarian cancer model to reconstruct KRAS oncogene-dependent cytoplasmic and transcriptional networks from perturbation experiments based on gene silencing and pathway inhibitor treatments. We measured mRNA and protein levels in manipulated cells by microarray, RT-PCR and Western Blot analysis, respectively. The reconstructed model revealed complex interactions among the transcriptional and cytoplasmic components, some of which were confirmed by double pertubation experiments. Interestingly, the transcription factors decomposed into two hierarchically arranged groups. To validate the model predictions we analysed growth parameters and transcriptional deregulation in the KRAS-transformed epithelial cells. As predicted by the model, we found two functional groups among the selected transcription factors. The experiments thus confirmed the predicted hierarchical transcription factor regulation and showed that the hierarchy manifests itself in downstream gene expression patterns and phenotype.
Publication Title
Reverse engineering a hierarchical regulatory network downstream of oncogenic KRAS.
Sample Metadata Fields
Cell line, Treatment
View Samples