This SuperSeries is composed of the SubSeries listed below.
Krüppel-like factor 4 (KLF4) inactivation in chronic lymphocytic leukemia correlates with promoter DNA-methylation and can be reversed by inhibition of NOTCH signaling.
Sex
View SamplesWhole genome sequencing revealed CLL as a disease of the genome and epigenome defined by somatic mutations and aberrant DNA-methylation. To uncover the impact of aberrant methylation on transcription, gene expression and methylation array profiling was performed in CLL and B-cells. RNA from 13 CLL patients and 6 healthy donor samples was analyzed on expression arrays.
Krüppel-like factor 4 (KLF4) inactivation in chronic lymphocytic leukemia correlates with promoter DNA-methylation and can be reversed by inhibition of NOTCH signaling.
Sex
View SamplesPilocytic astrocytomas (PA) are the most common brain tumor in pediatric patients and can cause significant morbidity, including chronic neurological deficiencies. They are characterized by activating alterations in the mitogen-activated protein kinase (MAPK) pathway, but little else is known about their development. To further define their molecular development, we analysed the global DNA methylation profiles of 61 PAs and 6 normal cerebellum samples and integrated this data with transcriptome profiling. These data revealed two subgroups of PA that separate according to tumor location (infratentorial versus supratentorial), and identified key neural developmental genes that are differentially methylated between the two groups. Significant expression differences were identified for the majority of differentially methylated genes, and these were unexpectedly associated with a strong positive correlation between methylation and expression. We also identified a large number of differentially methylated/expressed genes between cerebellar PAs and normal cerebellum, which included additional developmental genes.
Differential expression and methylation of brain developmental genes define location-specific subsets of pilocytic astrocytoma.
Sex, Specimen part
View SamplesInhibition of Brd4 with Jq1 in neurons with or without BDNF stimulation Overall design: Examination of the effects of Jq1 treatment on primary mouse cortical neurons
BET protein Brd4 activates transcription in neurons and BET inhibitor Jq1 blocks memory in mice.
No sample metadata fields
View SamplesWidespread epigenetic disruptions in FXS mice leads to transcriptional changes that likely contribute to the neuronal phenotpyes underlying FXS. Overall design: 7DIV cultured cortical neurons from WT or Fmr1 KO mice were treated for 24 hours with vehicle, Jq1, or THZ, performed in triplicate.
Excess Translation of Epigenetic Regulators Contributes to Fragile X Syndrome and Is Alleviated by Brd4 Inhibition.
Treatment, Subject
View SamplesWe used high throughput sequencing to analyze the transcriptional profiling of EVT. By comparing the transcriptional profiling of EVT with or without H19 knockdown, numerous genes showed significantly altered expression as a result of H19 repression. Overall design: HTR cells were transfected with either control siRNA or siH19. 48h later after transfection, total RNA was extracted for library preparation and RNA-seq analysis to compare trancript profiles between siCon and siH19 cells.
H19 long noncoding RNA alters trophoblast cell migration and invasion by regulating TβR3 in placentae with fetal growth restriction.
Cell line, Subject, Time
View SamplesIMR-32 cells were subjected to lentiviral YRNA infection or nELAVL RNAi and/or UV stress followed by RNAseq analysis to monitor RNA level changes Overall design: RNA from IMR-32 cells was Trizol extracted, Ribominus selected and submitted for high-throughput sequencing.
Regulatory consequences of neuronal ELAV-like protein binding to coding and non-coding RNAs in human brain.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Chd7 is indispensable for mammalian brain development through activation of a neuronal differentiation programme.
Specimen part, Treatment
View SamplesWe performed array-based expression profiling to determine genes regulated by Chd7 and Top2b in CGNs. Our data show Chd7 and Top2b coregulate a common set of neuronal genes.
Chd7 is indispensable for mammalian brain development through activation of a neuronal differentiation programme.
Specimen part, Treatment
View SamplesGlioblastoma (GBM) is an incurable brain tumor carrying a dismal prognosis, which displays considerable heterogeneity. We have recently identified recurrent H3F3A mutations affecting two critical positions of histone H3.3 (K27, G34) in one-third of pediatric GBM. Here we show that each of these H3F3A mutations defines an epigenetic subgroup of GBM with a distinct global methylation pattern, and are mutually exclusive with IDH1 mutation (characterizing a CpG-Island Methylator Phenotype (CIMP) subgroup). Three further epigenetic subgroups were enriched for hallmark genetic events of adult GBM (EGFR amplification, CDKN2A/B deletion) and/or known transcriptomic signatures. We also demonstrate that the two H3F3A mutations give rise to GBMs in separate anatomic compartments, with differential regulation of OLIG1/2 and FOXG1, possibly reflecting different cellular origins.
Hotspot mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of glioblastoma.
Sex
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