This SuperSeries is composed of the SubSeries listed below.
Cinacalcet inhibits neuroblastoma tumor growth and upregulates cancer-testis antigens.
Specimen part, Treatment
View SamplesCaSR modulation inhibits neuroblastoma growth
Cinacalcet inhibits neuroblastoma tumor growth and upregulates cancer-testis antigens.
Specimen part, Treatment
View SamplesCaSR modulation inhibits neuroblastoma growth
Cinacalcet inhibits neuroblastoma tumor growth and upregulates cancer-testis antigens.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
DNA methylation fingerprint of neuroblastoma reveals new biological and clinical insights.
Specimen part
View SamplesDNA methylation changes in neuroblastoma, a clinically-heterogeneous pediatric tumor, have been described essentially in promoter regions. We analyzed the DNA methylome of neuroblastoma using high-density microarrays and observed differential methylation not only in promoters but also in intragenic and intergenic regions at both CpG and non-CpG sites. These epigenetic changes showed a non-random distribution relative functional chromatin domains, and targeted development and cancer-related genes, relevant for neuroblastoma pathogenesis. CCND1, a gene overexpressed in neuroblastoma, showed hypomethylation of gene-body and upstream regulatory regions. Furthermore, tumors with diverse clinical-risk showed clear differences affecting CpG and, remarkably, non-CpG sites. Non-CpG methylation was present in clinically-favorable tumors and affected genes such as ALK, where non-CpG methylation correlated with low gene expression. Finally, we identified CpG and non-CpG methylation signatures which correlated with patients age at time-points relevant for neuroblastoma clinical behavior, and targeted genes related to neural development and neural crest regulatory network
DNA methylation fingerprint of neuroblastoma reveals new biological and clinical insights.
Specimen part
View SamplesMHC-I overexpression in muscle biopsies is a hallmark of inflammatory myopathies.However the mechanisms of MHC-I overexpression in each disease is not well understood. Microarray analysis from MHC-I-microdissected myofibers showed a differential expression signature in each inflammatory myopathy. Innate immunity and IFN-I pathways are upregulated vs healthy controls, specifically in dermatomyositis (DM).
Altered RIG-I/DDX58-mediated innate immunity in dermatomyositis.
Specimen part, Disease
View SamplesThe purpose of our study was to identify expression signatures and molecular markers associated with tumor recurrence and survival in patients with locally advanced head and neck squamous cell carcinoma (HNSCC).
Gene expression signatures and molecular markers associated with clinical outcome in locally advanced head and neck carcinoma.
Sex, Specimen part
View SamplesThis study identified genomwide KCl inducible readthrough transcription. The project also includes a Cap-Seq experiment to identify transcriptional start sites, demonstrating that KCl does not activate downstream transcriptional start sites, but indeed does induce readthrough
Widespread Inducible Transcription Downstream of Human Genes.
No sample metadata fields
View SamplesIllumina RNA-Seq of the nuclear RNA fraction (total RNA, no poly(A) selection from NIH3T3 cells treated with heat shock, osmotic stress, or oxidative stress
No associated publication
Sex, Specimen part, Treatment
View SamplesWe used microarrays to detail the global gene expression signature of PDAC and to identify distinct up- and down-regulated transcripts in these tumors compared to control pancreas. We also established from this dataset the metabolic signature of PDAC in order to define new metabolic therapeutic target for pancreatic cancer.
Cholesterol uptake disruption, in association with chemotherapy, is a promising combined metabolic therapy for pancreatic adenocarcinoma.
Sex, Age, Specimen part
View Samples