To search for rapid changes in gene expression following BCR activation, we performed DNA microarray analysis of activated splenic B cells with and without anti-IgM treatment for 3 hour. The expression of a remarkably large set of genes differed significantly.
Initiation of antigen receptor-dependent differentiation into plasma cells by calmodulin inhibition of E2A.
Age, Specimen part
View SamplesCentral nervous system primitive neuroectodermal tumors (CNS PNET) and medulloblastomas are both embryonal tumors that predominantly occur in children.
The role of the WNT/β-catenin pathway in central nervous system primitive neuroectodermal tumours (CNS PNETs).
No sample metadata fields
View SamplesThe gene expression patterns of favorable histology Wilms tumors (FHWT) that relapsed were compared with those that did not relapse using oligonucleotide arrays
Predicting relapse in favorable histology Wilms tumor using gene expression analysis: a report from the Renal Tumor Committee of the Children's Oncology Group.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Comparative expression analysis reveals lineage relationships between human and murine gliomas and a dominance of glial signatures during tumor propagation in vitro.
Sex, Age, Specimen part, Disease stage
View SamplesIn this study, we screened a cohort of 57 paediatric brain tumours, with a wide range of pathologies to identify gene expression profiles
Comparative expression analysis reveals lineage relationships between human and murine gliomas and a dominance of glial signatures during tumor propagation in vitro.
Sex, Age, Specimen part, Disease stage
View SamplesGain-of-function mutations in exon 3 of beta-catenin (CTNNB1) are specific for Wilms' tumors that have lost WT1, but 50% of WT1-mutant cases lack such "hot spot" mutations. To ask whether stabilization of beta-catenin might be essential after WT1 loss, and to identify downstream target genes, we compared expression profiles in WT1-mutant versus WT1 wild-type Wilms' tumors. Supervised and nonsupervised hierarchical clustering of the expression data separated these two classes of Wilms' tumor. The WT1-mutant tumors overexpressed genes encoding myogenic and other transcription factors (MOX2, LBX1, SIM2), signaling molecules (TGFB2, FST, BMP2A), extracellular Wnt inhibitors (WIF1, SFRP4), and known beta-catenin/TCF targets (FST, CSPG2, CMYC). Beta-Catenin/TCF target genes were overexpressed in the WT1-mutant tumors even in the absence of CTNNB1 exon 3 mutations, and complete sequencing revealed gain-of-function mutations elsewhere in the CTNNB1 gene in some of these tumors, increasing the overall mutation frequency to 75%. Lastly, we identified and validated a novel direct beta-catenin target gene, GAD1, among the WT1-mutant signature genes. These data highlight two molecular classes of Wilms' tumor, and indicate strong selection for stabilization of beta-catenin in the WT1-mutant class. Beta-Catenin stabilization can initiate tumorigenesis in other systems, and this mechanism is likely critical in tumor formation after loss of WT1.
CTNNB1 mutations and overexpression of Wnt/beta-catenin target genes in WT1-mutant Wilms' tumors.
No sample metadata fields
View SamplesMedulloblastoma is the most common malignant pediatric brain tumor, and mechanisms underlying its development are poorly understood. We identified recurrent amplification of the miR-17/92 polycistron proto-oncogene in 6% of pediatric medulloblastomas by high-resolution single-nucleotide polymorphism genotyping arrays and subsequent interphase fluorescence in situ hybridization on a human medulloblastoma tissue microarray. Profiling the expression of 427 mature microRNAs (miRNA) in a series of 90 primary human medulloblastomas revealed that components of the miR-17/92 polycistron are the most highly up-regulated miRNAs in medulloblastoma. Expression of miR-17/92 was highest in the subgroup of medulloblastomas associated with activation of the sonic hedgehog (Shh) signaling pathway compared with other subgroups of medulloblastoma. Medulloblastomas in which miR-17/92 was up-regulated also had elevated levels of MYC/MYCN expression. Consistent with its regulation by Shh, we observed that Shh treatment of primary cerebellar granule neuron precursors (CGNP), proposed cells of origin for the Shh-associated medulloblastomas, resulted in increased miR-17/92 expression. In CGNPs, the Shh effector N-myc, but not Gli1, induced miR-17/92 expression. Ectopic miR-17/92 expression in CGNPs synergized with exogenous Shh to increase proliferation and also enabled them to proliferate in the absence of Shh. We conclude that miR-17/92 is a positive effector of Shh-mediated proliferation and that aberrant expression/amplification of this miR confers a growth advantage to medulloblastomas.
The miR-17/92 polycistron is up-regulated in sonic hedgehog-driven medulloblastomas and induced by N-myc in sonic hedgehog-treated cerebellar neural precursors.
Sex, Age, Specimen part
View SamplesA major part of plant immune response is mediated by signaling pathways controlled by three hormnes, jasmonate, ethylene, and salicylate. The involvement of each of these hormone signaling pathways in Arabidopsis thaliana was investigated in response to infection of a necrotrophic fungal pathogen, A. brassicicola. Arabideopsis mutants deficient in these hormone signaling pathways were compared to wild type.
Arabidopsis PECTIN METHYLESTERASEs contribute to immunity against Pseudomonas syringae.
Specimen part
View SamplesLiver fibrosis is characterized by the excessive formation and accumulation of matrix proteins as a result of wound healing in the liver. A main event during fibrogenesis is the activation of the liver resident quiescent hepatic stellate cell (qHSC). Recent studies suggest that reversion of the activated HSC (aHSC) phenotype into a quiescent-like phenotype could be a major cellular mechanism underlying fibrosis regression in the liver, thereby offering new therapeutic perspectives for the treatment of liver fibrosis. The goal of the present study is to identify experimental conditions that can revert the activated status of human HSCs and to map the molecular events associated with this phenotype reversion by gene expression profiling
In vitro reversion of activated primary human hepatic stellate cells.
Sex, Age, Specimen part, Subject
View SamplesThe primary objective of the study was to investigate the uncoupling protein-1 (UCP1) associated features of human epicardial adipose tissue (eAT) using next generation deep sequencing. In addition, paired mediastinal adipose tissue (mAT) and subcutaneous adipose tissue (sAT) samples colleced from patients undergoing cardic surgeries at our center were included in the study. Overall design: Paired biopsies of eAT, mAT and sAT obtained from cardiac surgery patients (n=10), with specific criteria of high- and low- expression of UCP1 in eAT, were subjected to RNA sequencing. While the primary objective was to compare high- vs. low UCP1 expression in eAT, our study design further allowed us to investigate depot- and disease specific transcriptomic shifts in these patients. Specifically, 10 patients provided 30 samples (n = 10 each for eAT, mAT and sAT) that could be compared based on depot specificity (n = 10), obesity (n = 5 lean, n = 5 obese) and coronary artery disease (CAD) (n = 6 CAD, 4 = Non-CAD).
UCP1 expression-associated gene signatures of human epicardial adipose tissue.
Disease, Disease stage, Subject
View Samples