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Links from GEO DataSets

Items: 11

1.

Epigenome analysis of neuroblastoma cell treated by NEN under normoxia and hypoxia

(Submitter supplied) Genome wide DNA methylation profiling of neuroblastoma cell SK-N-BE(2) treated by 1µM NEN under normoxia and hypoxia for 24hrs. The IInfinium Human MethylationEPIC BeadChip v1.0 B5 was used to obtain DNA methylation profiles across approximately 850,000 methylation sites in the genome of neuroblastoma. Samples included 4 group with 3 biological replicates: (1) normoxia_CTRL (2) normoxia_NEN (3) hypoxia_CTRL (4) hypoxia_NEN
Organism:
Homo sapiens
Type:
Methylation profiling by array
Platform:
GPL21145
12 Samples
Download data: IDAT, TXT
Series
Accession:
GSE211558
ID:
200211558
2.

Transcriptome changes after NEN treament in neuroblastoma cell

(Submitter supplied) To study the gene expression changes after niclosamide ethanolamine (NEN) treament in neuroblastoma cell, we treated SK-N-BE(2) with 1µM NEN for 24hours. The RNA were extracted from the cells and submitted for RNA sequencing.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: TXT
Series
Accession:
GSE209801
ID:
200209801
3.

Transcription factor activating protein 2 beta (TFAP2B) mediates noradrenergic neuronal differentiation in neuroblastoma

(Submitter supplied) Single-color gene expression profiles from IMR-32 neuroblastoma cell lines were generated using 44K oligonucleotide microarrays. To gain insights into the molecular processes occurring upon TFAP2B re-expression, we performed gene expression measurements in TFAP2B and GFP expressing transgenic IMR-32 neuroblastoma cell lines at d2 and d7 of transgene induction.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16876
4 Samples
Download data: TXT
Series
Accession:
GSE74350
ID:
200074350
4.

Transcriptomic analysis of neuroblastoma SH-SY5Y cells in response to stable over-expression of neuroblastoma highly expressed 1 (NHEG1)

(Submitter supplied) Neuroblastoma (NB), a malignant embryonic tumor arising from primitive neural crest cells, accounts for more than 7% of malignancies and around 15% of cancer-related mortality in childhood. Better elucidating the mechanisms of tumorigenesis and aggressiveness is important for improving the therapeutic efficiencies of NB. Through mining public microarray and RNA sequencing datasets, we identified neuroblastoma highly expressed 1 (NHEG1) as a novel 1360-bp lncRNA associated with poor outcome of NB. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17586
6 Samples
Download data: CEL
Series
Accession:
GSE80393
ID:
200080393
5.

Gene expression profiling of TH-MYCN mouse neuroblastoma sphere cells and their parental primary tumor cells

(Submitter supplied) We performed microarray gene expression profiling to identify genes essential for the growth and tumorigenicity of mouse neuroblastoma stem-like cells
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
6 Samples
Download data: CEL
Series
Accession:
GSE80252
ID:
200080252
6.

DNMT3B7, an aberrant DNMT3B isoform, suppresses growth, induces differentiation, and alters DNA methylation in human neuroblastoma

(Submitter supplied) In adult cancers, epigenetic changes and aberrant splicing of the DNMT3B is commonly observed, and the pattern of gene methylation and expression has been shown to be modified by DNMT3B7, a truncated protein of DNMT3B. Much less is known about the mechanism of epigenetic changes in the pediatric cancer neuroblastoma. To investigate if aberrant DNMT3B transcripts alter DNA methylation, gene expression and tumor phenotype in neuroblastoma, we measured DNMT3B isoform expression in primary tumors and cell lines. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL9115
3 Samples
Download data: TAR
7.

EZH2 regulates neuroblastoma cell differentiation via NTRK1 promoter epigenetic modifications

(Submitter supplied) The polycomb repressor complex 2 molecule EZH2 is now known to play a role in essential cellular processes, namely, cell fate decisions, cell cycle regulation, senescence, cell differentiation, and cancer development/progression. EZH2 inhibitors have recently been developed; however, their effectiveness and underlying molecular mechanisms in many malignancies have not yet been elucidated in detail. Although the functional role of EZH2 in tumorigenesis in neuroblastoma (NB) has been investigated, mutations of EZH2 have not been reported. A Kaplan-Meier analysis on the event free- and overall survival of NB patients indicated that the highexpression of EZH2 correlated with an unfavorable prognosis. In order to elucidate the functional roles of EZH2 in NB tumorigenesis and its aggressiveness, we knocked down EZH2 in NB cell lines using lentivirus systems. The knockdown of EZH2 significantly induced NB cell differentiation, e.g. neurite extension, and the neuronal differentiation markers, NF68 and GAP43. EZH2 inhibitors also induced NB cell differentiation. We performed a comprehensive transcriptome analysis using Human Gene Expression Microarrays and found that NTRK1 (TrkA) is one of the EZH2-related suppression targets. The depletion of NTRK1 canceled EZH2 knockdown-induced NB cell differentiation. Our integrative methylome, transcriptome, and chromatin immunoprecipitation assays using NB cell lines and clinical samples clarified that the NTRK1 P1 and P2 promoter regions were regulated differently by DNA methylation and EZH2-related histone modifications. The NTRK1 transcript variants 1/2, which were regulated by EZH2-related H3K27me3 modifications at the P1 promoter region, were strongly expressed in favorable, but not unfavorable NB. The depletion and inhibition of EZH2 successfully induced NTRK1 transcripts and functional proteins. Collectively, these results indicate that EZH2 plays important roles in preventing the differentiation of NB cells and also that EZH2-related NTRK1 transcriptional regulation may be the key pathway for NB cell differentiation.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16699
18 Samples
Download data: TXT
Series
Accession:
GSE98642
ID:
200098642
8.

Combined epigenetic and differentiation-based treatment inhibits neuroblastoma tumor growth and links HIF2α to tumor suppression

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Methylation profiling by genome tiling array
Platforms:
GPL13534 GPL11154
90 Samples
Download data: IDAT, TXT
Series
Accession:
GSE102996
ID:
200102996
9.

Combined epigenetic and differentiation-based treatment inhibits neuroblastoma tumor growth and links HIF2α to tumor suppression [array]

(Submitter supplied) Neuroblastoma is a pediatric cancer characterized by variable outcomes ranging from spontaneous regression to life-threatening progression. High-risk neuroblastoma patients receive myeloablative chemotherapy with hematopoietic stem-cell transplant followed by adjuvant retinoid differentiation treatment. However, the overall survival remains low; hence, there is an urgent need for alternative therapeutic approaches. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL13534
22 Samples
Download data: IDAT, TXT
Series
Accession:
GSE102994
ID:
200102994
10.

Combined epigenetic and differentiation-based treatment inhibits neuroblastoma tumor growth and links HIF2α to tumor suppression [RNA-Seq]

(Submitter supplied) Neuroblastoma is a pediatric cancer characterized by variable outcomes ranging from spontaneous regression to life-threatening progression. High-risk neuroblastoma patients receive myeloablative chemotherapy with hematopoietic stem-cell transplant followed by adjuvant retinoid differentiation treatment. However, the overall survival remains low; hence, there is an urgent need for alternative therapeutic approaches. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
68 Samples
Download data: TXT
11.

Combination therapies induce cancer cell death through the integrated stress response and disturbed pyrimidine metabolism

(Submitter supplied) By accentuating drug efficacy and impeding resistance mechanisms, combinatorial, multi-agent therapies have emerged as key approaches in the treatment of complex diseases, most notably cancer. Using high-throughput drug screens, we uncovered distinct metabolic vulnerabilities and thereby identified drug combinations synergistically causing a starvation-like lethal catabolic response in tumor cells from different cancer entities. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL24324
12 Samples
Download data: CEL
Series
Accession:
GSE148682
ID:
200148682
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