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1,258 results for “neuroblastoma”
Differential gene expression in neuroblastoma cells after transfection with control siRNA or linc00467 siRNA
GEO Series GSE52985. Homo sapiens. 2 samples. Type: Expression profiling by array.
Retinoic acid-induced neuroblastoma cells
GEO Series GSE1596. Mus musculus. 13 samples. Type: Expression profiling by array.
Impact of NRSF variant over-expression in SK-N-AS human neuroblastoma cells
GEO Series GSE22467. Homo sapiens. 9 samples. Type: Expression profiling by array.
TH-MYCN Mice with Caspase-8 Deficiency Develop Advanced Neuroblastoma with Bone Marrow Metastasis
Neuroblastoma, the most common extracranial pediatric solid tumor, is responsible for 15% of all childhood cancer deaths. Patients frequently present at diagnosis with metastatic disease, particularly to the bone marrow. Advances in therapy and understanding of the metastatic process have been limited due in part, to the lack of animal models harboring bone marrow disease. The widely employed transgenic model, the TH-MYCN mouse, exhibits limited metastasis to this site. Here we establish the first genetic immunocompetent mouse model for metastatic neuroblastoma with enhanced secondary tumors in the bone marrow.
Transient treatment with epigenetic modifiers yields stable neuroblastoma stem cells resembling aggressive large-cell neuroblastomas
Cancer stem cells are plastic in nature, a characteristic that hampers cancer therapeutics. Neuroblastoma (NB) is a pediatric tumor of neural crest origin, and half of the cases are highly aggressive. By treating NB cell lines (SKNAS, SKNBE(2)C, CHP134, SY5Y) with epigenetic modifiers for a short time followed by sphere-forming culture conditions, we have established stem cell-like NB cells that are phenotypically stable for over a year.
GRHL1 acts as a tumor suppressor in neuroblastoma and is negatively regulated by MYCN and HDAC3
Neuroblastoma is an embryonic solid tumor of neural crest origin and accounts for 11% of all cancer-related deaths in children. Novel therapeutic strategies are therefore urgently required. MYCN oncogene amplification, which occurs in 20% of neuroblastomas, is a hallmark of high risk. Here we aimed to exploit molecular mechanisms that can be pharmacologically addressed with epigenetically modifying drugs, such as histone deacetylase (HDAC) inhibitors. GRHL1, a gene critical for Drosophila neural development, belonged to the genes most strongly responding to HDAC inhibitor treatment of neuroblastoma cells in a genome- wide screen. An increase in the histone H4 pan-acetylation associated with its promoter preceded transcriptional activation. Physically adjacent, HDAC3 and MYCN co-localized to the GRHL1 promoter and repressed its transcription. High-level GRHL1 expression in primary neuroblastomas correlated on transcriptional and translational levels with favorable patient survival and established clinical and molecular markers for favorable tumor biology, including lack of MYCN amplification. Enforced GRHL1 expression in MYCN-amplified neuroblastoma cells with low endogenous GRHL1 levels abrogated anchorage-independent colony formation, inhibited proliferation and retarded xenograft growth in mice. GRHL1 regulated 170 genes genome-wide, and most were involved in pathways regulated during neuroblastomagenesis, including nervous system development, proliferation, cell-cell adhesion, cell spreading and cellular differentiation. In summary, the data presented here indicate a significant role of HDAC3 in the MYCN-mediated repression of GRHL1 and suggest drugs that block HDAC3 activity and suppress MYCN expression as promising candidates for novel treatment strategies of high-risk neuroblastoma.
Genome-wide SNP Profiling of 27 Neuroblastoma Cell Lines
We used SNP arrays to perform genome-wide profiling of commonly-used neuroblastoma cell lines.
Italian Neuroblastoma Registry
The Italian Neuroblastoma Registry was activated in 1979 and includes all subjects with any peripheral neuroblastic tumor (PNT, ie, neuroblastoma, ganglioneuroblastoma, and the benign ganglioneuroma), diagnosed at the institutions participating in the Italian Neuroblastoma Group (ING).11 In the last decade more than 90% of the expected Italian PNTs have been recruited through this network. Children age 0 to 14 years diagnosed with malignant PNT between January 1979 and December 2005 were eligible. Older children were excluded because 14 years of age was the limit for admission to most Italian pediatric institutions.
Identification of drug-resistance-related cell states in paired pre- and post-treatment neuroblastoma cell lines
For more information, including a more complete description, data generator contact information, and reference, please see: https://scpca.alexslemonade.org/projects/SCPCP000020.
Identification of drug-resistance-related cell states in paired pre- and post-treatment neuroblastoma PDXs
For more information, including a more complete description, data generator contact information, and reference, please see: https://scpca.alexslemonade.org/projects/SCPCP000024.
Neuroblastoma U Cologne
Whole-genome sequencing of 56 neuroblastoma tumor/normal pairs.
Transcriptome Sequencing of Pediatric Neuroblastoma
Neuroblastoma is the most common extra-cranial solid tumor in children. It represents 8% to 10% of all childhood cancers. Stage 4 Neuroblastoma is characterized by its clinical heterogeneous outcome. The special category, stage 4S tumors (2-5% of all NB) are chemo-sensitive, and the patients show spontaneous regression. On the other hand, MYCN amplification (25-30% of all NB) is associated with poor outcome of neuroblastoma, thus we further categorize stage 4 neuroblastoma into MYCN non-amplified and MYCN amplified group. Here we use transcriptome sequencing to characterize the transcriptome in 29 stage 4 Neuroblastoma samples.
PEDS-PLAN - Pediatric Precision Laboratory Advanced Neuroblastoma Therapy
A multi-center clinical trial for newly diagnosed high-risk neuroblastoma patients. Molecular tumor boards selected one of six targeted agents based on tumor-normal whole exome sequencing and tumor RNA sequencing data.
TARGET: Neuroblastoma (NBL)
There are ~214 fully characterized patient cases with neuroblastoma (all tumor/normal pairs, 10 with relapse sample as well) that will make up the TARGET NBL dataset, along with some cell lines and xenografts. The dataset includes 24 4S cases as well. Each fully characterized case has gene expression, tumor and paired normal copy number analyses, methylation and comprehensive next-generation sequencing to include whole genome and/or whole exome sequencing. A majority of these cases will also have mRNA-seq and methylation data available as well. There are additionally a large number of cases, both low and high risk, with partial molecular characterization to include some next generation and targeted Sanger sequencing making this a large and informative genomic dataset.
Clonal evolution during metastatic spread in high-risk neuroblastoma
Patients with high-risk neuroblastoma (HR-NB) frequently present with widely metastatic disease with tumors harboring recurrent MYCN, TERT and ATRX alterations. Most genomic studies to-date, however, have focused on single diagnostic samples. Consequently our understanding of the clonal and genetic evolution of disease progression and metastasis remains limited. We set out to deliver a detailed characterization of clonal architecture of HR-NB during disease evolution and identify the biological pathways important for progression. We studied 470 sequential and spatially separated samples from 283 patients. This particular dbGAP study contains data from 182 tumors from 68 individuals. For 30 individuals (72 tumors with WGS and 70 tumors with RNA-seq) raw WGS/RNA-seq data and somatic mutation calls are available. For 38 individuals (n=110 tumors) somatic mutation calls are available.
Pediatric In Vivo Testing Program - Neuroblastoma
Children with disseminated neuroblastoma have a very high risk of treatment failure and death despite receiving intensified chemotherapy, radiation therapy and immunotherapy. The long-term goal of the Mossé and Maris translational research programs is to substantively improve neuroblastoma cure rates by developing patient-specific therapies that target the unique oncogenic drivers of each case.
Pediatric In Vivo Testing Program - Neuroblastoma
Open the record for dataset details and reuse information.
HuD regulates SOD1 expression during oxidative stress in differentiated neuroblastoma cells and sporadic ALS motor cortex
<p><strong>The database includes </strong>the raw of the article “HuD regulates SOD1 expression during oxidative stress in differentiated neuroblastoma cells and sporadic ALS motor cortex”.</p> <p><strong>In detail, the database contains</strong> data obtained by the following evaluations: i) RNA electrophoretic mobility shift assay (REMSA) to detect the formation of a complex between HuD recombinant protein and SOD1 ARE sequences. ii) multiplex qRT-PCR to evaluate if oxidative stress levels, i.e H2O2 treatment, induces a shift in the alternative polyadenylation (APA) site usage in SOD1 3'UTR.</p> <p><strong>Aim of the work</strong> was to investigate the potential involvement of HuD (ELAVL4) one of the neuronal members of the ELAVL family, in SOD1 regulation during oxidative stress and in sporadic ALS patients (sALS).</p> <p>Using differentiated SH-SY5Y cells along with brain tissues from sALS patients, we evaluated HuD-dependent regulation of SOD1 mRNA. By means in vitro binding and mRNA decay assays we observed that HuD specifically binds to SOD1 ARE motifs promoting mRNA stabilization. In SH-SY5Y cells, we faound that the overexpression of full-length HuD increased SOD1 mRNA and protein levels; moreover HuD regulation of SOD1 mRNA we found that this regulation is related to oxidative stress, as shown after H2O2 exposure. H2O2 exposure also induced a shift in the APA site usage in SOD1 3'UTR, increasing the levels of a long variant bearing HuD binding sites. We validated this data using a specific siRNA. In the motor cortex from sALS patients, we found increases in SOD1 and HuD mRNAs and proteins, accompanied by greater HuD binding to this mRNA as confirmed by RNA-immunoprecipitation (RIP) assays.</p> <p><strong>To conclude,</strong> these results point a role of HuD in the post-transcriptional regulation of SOD1 expression in neurons after oxidative stress and in sALS brain tissues, thus suggesting an involvement in ALS pathogenesis.</p>
Discovery of Dual targeting PEGylated BG-P1600-TAT to Norepinephrin Transporter (NET) and Thyrointegrin αvβ3 in the Treatment of Neuroblastoma cancer cellline
GEO Series GSE183482. Homo sapiens. 10 samples. Type: Expression profiling by array.
Neuroblastoma Neuro2A Cell Differentiation induced by retinoic acid-treatment
GEO Series GSE2570. Mus musculus. 38 samples. Type: Expression profiling by array.
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.