We used microarrays to study the changes in the transcriptional profile upon Snail knockdown in murine lung adenocarcinomas
Snail mediates repression of the Dlk1-Dio3 locus in lung tumor-infiltrating immune cells.
Age, Specimen part
View SamplesWe used microarrays to study the changes in the transcriptional profile upon Snail overexpression in murine lung adenocarcinomas
Snail mediates repression of the Dlk1-Dio3 locus in lung tumor-infiltrating immune cells.
Age, Specimen part
View SamplesEvaluation of the role of RIP4 in lung adenocarcinoma revealed that RIP4 inhibits STAT3 signaling in vitro and in vivo. Repression of RIP4 enhanced STAT3 signaling activation in KRAS LSL/G12D/wt; p53flox/flox murine tumors. This promoted cancer dedifferentiation through ECM remodeling
RIP4 inhibits STAT3 signaling to sustain lung adenocarcinoma differentiation.
Age, Specimen part
View SamplesOne current focus of nutrition research is the identification of biomarkers that reflect the impact of food on metabolic processes. As this approach mostly targets the prevention rather than the curing of diseases, novel biomarkers need to be identified. Those should be influenced by the diet already in healthy individuals and be nonetheless indicative, or even predictive, of the potential impact of specific food on the development of metabolic diseases such as obesity.
Caloric dose-responsive genes in blood cells differentiate the metabolic status of obese men.
Specimen part
View SamplesLymphatic valves are specialized units regularly distributed along collecting vessels that allow unidirectional forward propulsion of the lymph, and its efficient transport from tissues to the bloodstream. Lymphatic endothelial cells that cover lymphatic valve sinuses are subjected to complex flow patterns, due to recirculation of the lymph during the collecting vessel pumping cycle. They also express high levels of FOXC2 transcription factor.
FOXC2 and fluid shear stress stabilize postnatal lymphatic vasculature.
Specimen part, Treatment
View SamplesTo identify the CAR-, PXR- and PPAR-specific genome-wide expression changes, hepatocyte cultures from six individual donors were treated with the prototypical ligands for
Genomewide comparison of the inducible transcriptomes of nuclear receptors CAR, PXR and PPARα in primary human hepatocytes.
Sex, Age
View SamplesStatins are widely used cholesterol-lowering drugs that inhibit HMG-CoA reductase, a key enzyme in cholesterol synthesis. In some cases, however, these drugs may cause a number of toxic side effects in hepatocytes and skeletal muscle tissue. Currently, the specific molecular mechanisms that cause these adverse effects are not sufficiently understood. In this work, genome-wide RNA expression changes in primary human hepatocytes of six individuals were measured at five time points upon atorvastatin treatment. A novel systems-level analysis workflow was applied to reconstruct regulatory mechanisms based on these drug-response data and available knowledge about transcription factor binding specificities, protein-protein interactions and protein-drug interactions. Several previously unknown transcription factors, regulatory cofactors and signaling molecules were found to be involved in atorvastatin-responsive gene expression. Some novel relationships, e.g., the regulatory influence of nuclear receptor NR2C2 on CYP3A4, were successfully validated in wet-lab experiments.
Inferring statin-induced gene regulatory relationships in primary human hepatocytes.
Specimen part, Treatment, Subject
View SamplesPurpose: The phosphoinositide 3-kinase (PI3K) pathway is fundamental for cell proliferation and survival and is frequently altered and activated in neoplasia, including carcinomas of the lung. In this study we investigated the potential of targeting the catalytic class IA PI3K isoforms in small cell lung cancer (SCLC), which is the most aggressive of all lung cancer types. Experimental Design: The expression of PI3K isoforms in patient specimens was analyzed. The effects on SCLC cell survival and downstream signaling were determined following PI3K isoform inhibition by selective inhibitors or down-regulation by small interfering RNA. Results: Over-expression of the PI3K isoforms p110 and p110 was shown by immunohistochemistry in primary SCLC tissue samples. Targeting the PI3K p110 with RNA interference (RNAi) or selective pharmacological inhibitors resulted in strongly affected cell proliferation of SCLC cells in vitro and in vivo, while targeting p110 was less effective. Inhibition of p110 also resulted in increased apoptosis and autophagy, which was accompanied by decreased phosphorylation of Akt and components of the mammalian target of rapamycin (mTOR) pathway, such as the ribosomal S6 protein, and the eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1). A DNA microarray analysis revealed that p110 inhibition profoundly affected the balance of pro- and anti-apoptotic Bcl-2 family proteins. Finally, p110 inhibition led to impaired SCLC tumor formation and vascularization in vivo. Conclusion: Together our data demonstrate the key involvement of the PI3K isoform p110 in multiple tumor-promoting processes in SCLC.
Targeting the phosphoinositide 3-kinase p110-α isoform impairs cell proliferation, survival, and tumor growth in small cell lung cancer.
Cell line, Treatment
View SamplesGene expression analysis identified a MLL translocation-specific signature of differentially expressed genes discriminating ALL and AML with and without MLL rearrangements.
MLL rearrangements in pediatric acute lymphoblastic and myeloblastic leukemias: MLL specific and lineage specific signatures.
No sample metadata fields
View SamplesExposure to Polychlorobiphenyls (PCBs) is known to cause serious health effects in human but the gene expression profiles leading to development of differnet diseases and disorders are not fully understood. The knowledge of global gene expression will help us to devlop early disease or disorder biomarkers for PCB induced health effects.
Global gene expression and Ingenuity biological functions analysis on PCBs 153 and 138 induced human PBMC in vitro reveals differential mode(s) of action in developing toxicities.
Sex, Age, Specimen part, Treatment
View Samples