Gene expression patterns of testicular seminoma were analysed applying oligonucleotide microarrays in 40 specimens of different tumour stages (pT1, pT2, pT3) and in 3 normal testes.
Gene signatures of testicular seminoma with emphasis on expression of ets variant gene 4.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
RNA sequencing validation of the Complexity INdex in SARComas prognostic signature.
Time
View SamplesWe validated the technological and material transfers of the CINSARC signature.
RNA sequencing validation of the Complexity INdex in SARComas prognostic signature.
Time
View SamplesOne of the main problems in managing desmoids tumors is their locoregional aggressiveness and their high ability to recur after initial treatment. In our work, with the goal to identify molecular markers that can predict Progression-Free Survival, gene-expression screening was conducted on 128 available independent untreated primary desmoid tumors using cDNA microarray. By analyzing expression profiles, we have identified, for the first time, a gene expression signature that is able to predict Progression-Free Survival. This molecular signature identified two groups with clearly distinct Progression-Free Survival in the two sets of subjects. Patients in good prognostic group had achieved a progression-free 2-year survival rate of 86% while patients in poor prognostic group had a progression-free 2-year survival rate of 44%.
Gene Expression Profiling of Desmoid Tumors by cDNA Microarrays and Correlation with Progression-Free Survival.
Sex, Age, Specimen part
View SamplesThe heat shock response (HSR) is a mechanism to cope with proteotoxic stress by inducing the expression of molecular chaperones and other heat shock response genes. The HSR is evolutionarily well conserved and has been widely studied in bacteria, cell lines and lower eukaryotic model organisms. However, mechanistic insights into the HSR in higher eukaryotes, in particular in mammals, are limited. We have developed an in vivo heat shock protocol to analyze the HSR in mice and dissected heat shock factor 1 (HSF1)-dependent and -independent pathways. Whilst the induction of proteostasis-related genes was dependent on HSF1, the regulation of circadian function related genes, indicating that the circadian clock oscillators have been reset, was independent of its presence. Furthermore, we demonstrate that the in vivo HSR is impaired in mouse models of Huntington's disease but we were unable to corroborate the general repression of transcription after a heat shock found in lower eukaryotes. Overall design: RNA-Seq was performed on mRNA isolated from quadriceps femoris muscle of 24 mice. These mice were of wild type, R6/2, and Hsf1-/- genotypes. Two mice of each genotype were tested in four conditions: (1) heat shock, (2) control heat shock, (3) HSP90 inhibition (NVP-HSP990), and (4) HSP90 inhibition vehicle.
HSF1-dependent and -independent regulation of the mammalian in vivo heat shock response and its impairment in Huntington's disease mouse models.
Age, Specimen part, Treatment, Subject
View SamplesNo description.
Genomic and transcriptomic comparison of post-radiation versus sporadic sarcomas.
No sample metadata fields
View SamplesNo description.
Genomic and transcriptomic comparison of post-radiation versus sporadic sarcomas.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesCaspase-8 is a cystein protease involved in regulating apoptosis. The function of caspase-8 was studied in the intestinal epithelium, using mice with an intestinal epithelial cell specific deletion of caspase-8.
Caspase-8 regulates TNF-α-induced epithelial necroptosis and terminal ileitis.
Specimen part
View SamplesPurpose: Transcriptome profiling (RNA-seq) to microarray to evaluate transcriptional changes in the heart of HD mouse models Methods: Heart mRNA profiles of 4-weeks-old wild-type (WT) and R6/2 transgenic; 15-weeks-old WT and R6/2 transgenic mice; 8-month-old WT and HdhQ150 knock-in mice; 22-month-old WT and HdhQ150 knock-in mice were generated by deep sequencing, in triplicate, using Illumina Hi-seq 2000. Conclusions: Our study showed that there is no major transcriptional deregulation in the heart of mouse models of HD. Overall design: Heart mRNA profiles of 4-weeks-old wild-type (WT) and R6/2 transgenic; 15-weeks-old WT and R6/2 transgenic mice; 8-month-old WT and HdhQ150 knock-in mice; 22-month-old WT and HdhQ150 knock-in mice were generated by deep sequencing, in triplicate, using Illumina Hi-seq 2000.
Dysfunction of the CNS-heart axis in mouse models of Huntington's disease.
No sample metadata fields
View SamplesCell Line: This experiment was designed to measure the transcriptional responses to four kinase inhibitors across a five-logarithm dose range. The A549 human lung cancer cell line was treated with dasatinib, imatinib or nilotinib (4 hours and 20 hours) or PD0325901 (4 hours). Treatments used a 12-point dose range (30 uM with 3-fold dilutions down to 0.17 nM; 0.5% DMSO vehicle for all treatments). Experimental design prevented row or column handling effects being confounded with dose effect.
Transcriptional profiling of the dose response: a more powerful approach for characterizing drug activities.
Disease, Cell line, Compound, Time
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