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GSE52989
Homo sapiens
24 Downloadable Samples
Affymetrix Human Genome U133A Array (hgu133a)
Description
To identify the molecular mechanisms and environmental inducers contributing to reprogramming of hepatocytes into progenitors in HCC context, we used the HepaRG cell line as model.
Publication Title
Inflammatory cytokines promote the retrodifferentiation of tumor-derived hepatocyte-like cells to progenitor cells.
Sample Metadata Fields
Cell line, Time
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
No associated publication
Sample Metadata Fields
Disease
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Peeling Skin Disease (PSD; OMIM 270300) is an inflammatory ichthyosis due to homozygous loss-of-function mutations in Corneodesmosin (CDSN) and characterized by lifelong patchy peeling of the skin associated with eczema, food allergy and severe itching. The pathophysiology of PSD is still poorly known. The initial event of the disease, the detachment of the SC due to a CDSN deficiency, leads to an impairment of the permeability barrier which could in turn trigger erythema, pruritus and atopic manifestations by mechanisms not entirely elucidated. Cdsn-deficient mouse models are interesting tools to decipher these underlying mechanisms. In order to explore the still poorly known pathophysiological mechanisms of PSD, we analyzed the cutaneous transcriptome of two epidermis-specific Cdsn-deficient mouse models representative of early (occurrence of the permeability defect in Cdsnep-/- E18.5 embryos) and chronic (permanent permeability defect in Cdsniep-/- adult mice) phases of the disease
Publication Title
No associated publication
Sample Metadata Fields
Disease
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Peeling Skin Disease (PSD; OMIM 270300) is an inflammatory ichthyosis due to homozygous loss-of-function mutations in Corneodesmosin (CDSN) and characterized by lifelong patchy peeling of the skin associated with eczema, food allergy and severe itching. The pathophysiology of PSD is still poorly known. The initial event of the disease, the detachment of the SC due to a CDSN deficiency, leads to an impairment of the permeability barrier which could in turn trigger erythema, pruritus and atopic manifestations by mechanisms not entirely elucidated. Cdsn-deficient mouse models are interesting tools to decipher these underlying mechanisms. In order to explore the still poorly known pathophysiological mechanisms of PSD, we analyzed the cutaneous transcriptome of two epidermis-specific Cdsn-deficient mouse models representative of early (occurrence of the permeability defect in Cdsnep-/- E18.5 embryos) and chronic (permanent permeability defect in Cdsniep-/- adult mice) phases of the disease
Publication Title
No associated publication
Sample Metadata Fields
Disease
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
The exposure to and contamination by Persistent Organic Pollutants (POPs), which include pesticides used worldwide and polyaromatic hydrocarbons, is detrimental to human health and diverse ecosystems. Although most mechanistic studies have focused on single compounds, living organisms are exposed to multiple environmental xenobiotics, simultaneously, throughout their lives. The experimental evidence useful for assessing the effects of exposure to pollutant mixtures is scarce. We investigated the effects of exposure to a combination of two POPs, which employ different xenosensors, on global gene expression in a human hepatocyte cell model, HepaRG.
Publication Title
Two persistent organic pollutants which act through different xenosensors (alpha-endosulfan and 2,3,7,8 tetrachlorodibenzo-p-dioxin) interact in a mixture and downregulate multiple genes involved in human hepatocyte lipid and glucose metabolism.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Analysis of genes that were differentially expressed in MSC-derived hES cells (VUB01 and SA01) as compared to VUB01 and SA01 undifferentiated hES cells
Publication Title
Combined mRNA and microRNA profiling reveals that miR-148a and miR-20b control human mesenchymal stem cell phenotype via EPAS1.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 90 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Hepatocellular carcinoma (HCC) is ranked second in cancer-associated deaths worldwide. Most cases of HCC are secondary to either a viral hepatitis infection (hepatitis B or C) or cirrhosis (alcoholism being the most common cause of hepatic cirrhosis). It is a complex and heterogeneous tumor due to activation of multiple cellular pathways and molecular alterations.
Publication Title
Exome sequencing of hepatocellular carcinomas identifies new mutational signatures and potential therapeutic targets.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Biallelic inactivating mutations of the transcription factor 1 gene (TCF1), encoding hepatocyte nuclear factor 1a (HNF1a), were identified in 50% of hepatocellular adenomas (HCA) phenotypically characterized by a striking steatosis. To understand the molecular basis of this aberrant lipid storage, we performed a microarray transcriptome analysis validated by quantitative RT-PCR, western-blotting and lipid profiling. In mutated HCA, we showed a repression of gluconeogenesis coordinated with an activation of glycolysis, citrate shuttle and fatty acid synthesis predicting elevated rates of lipogenesis. Moreover, the strong dowregulation of L-FABP suggests that impaired fatty acid trafficking may also contribute to the fatty phenotype. In addition, transcriptional profile analysis of the observed deregulated genes in non-HNF1a-mutated HCA as well as in non-tumor livers allowed us to define a specific signature of the HNF1a-mutated HCA. In theses tumors, lipid composition was dramatically modified according to the transcriptional deregulations identified in the fatty acid synthetic pathway. Surprisingly, lipogenesis activation did not operate through SREBP-1 and ChREBP that were repressed. We conclude that steatosis in HNF1a-mutated HCA results mainly from an aberrant promotion of lipogenesis that is linked to HNF1a inactivation and that is independent of both SREBP-1 and ChREBP activation. Finally, our findings have potential clinical implications since lipogenesis can be efficiently inhibited by targeted therapies.
Publication Title
HNF1alpha inactivation promotes lipogenesis in human hepatocellular adenoma independently of SREBP-1 and carbohydrate-response element-binding protein (ChREBP) activation.
Sample Metadata Fields
Sex, Specimen part, Disease
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Focal nodular hyperplasias (FNHs) are benign liver lesions considered to be a hyperplastic response to increased blood flow in otherwise normal liver. In contrast, FNH-like nodules occur in cirrhotic liver but share similar histopathological features. To better understand the pathophysiology of FNH, we performed a transcriptomic analysis. Methods: Affymetrix and cDNA microarrays were used to compare gene expression in eight FNHs with that in tissue from six normal livers. Selected genes were validated with quantitative RT-PCR in 70 benign liver tumors including adenomas and cirrhotic and FNH-like lesions. Results: Among the deregulated genes in FNHs, 19 were physiologically zonated in the normal liver lobule. All six periveinous genes were up-regulated in FNH, whereas 13 genes normally expressed in the periportal area were down-regulated. Immunohistochemistry revealed that glutamine synthetase was markedly overexpressed, forming anastomosed areas usually centered on visible veins. -catenin mRNA was slightly but significantly overexpressed, as were several known -catenin target genes. Moreover, activated hypophosphorylated -catenin protein accumulated in FNH in the absence of activating mutations. These results suggest zonated activation of the -catenin pathway specifically in FNH, whereas the other benign hepatocellular tumors, including FNH-like lesions, demonstrated an entirely different pattern of -catenin expression. Conclusions: In FNH, increased expression of the -catenin pathway was restricted to enlarged periveinous areas, which may explain the slight polyclonal over-proliferation of hepatocytes at the origin of the lesion. FNH-like nodules may have a different pathogenetic origin.
Publication Title
The beta-catenin pathway is activated in focal nodular hyperplasia but not in cirrhotic FNH-like nodules.
Sample Metadata Fields
Sex, Specimen part, Disease
View Samples- Homo sapiens
- 17 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The transcriptome analysis was performed in triplicate using two human embryonic stem cells lines (hES_VUB01 and hES_SA01) by comparing the expression profiles of the undifferentiated hES cells and two types of progenitors derived from the hES cell lines: Neural progenitors (NPC) and Mesodermal progenitors (MSC).
Publication Title
Global transcriptional profiling of neural and mesenchymal progenitors derived from human embryonic stem cells reveals alternative developmental signaling pathways.
Sample Metadata Fields
No sample metadata fields
View Samples