U.S. flag

An official website of the United States government

Format
Items per page
Sort by

Send to:

Choose Destination

Links from GEO DataSets

Items: 20

1.

Myc-driven medulloblastoma cells treated with Panobinostat (LBH589)

(Submitter supplied) Mouse MycT58A/DNp53 (MP) medulloblastoma cells were treated with DMSO or HDAC inhibitor (HDACi) panobinostat for 6 or 12 hours in vitro. Gene expression profiling was performed to compare cells treated with panobinostat and DMSO.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
12 Samples
Download data: CEL, CHP
Series
Accession:
GSE69410
ID:
200069410
2.

An Animal Model of Myc-driven medulloblastoma

(Submitter supplied) Medulloblastoma (MB) is the most common malignant brain tumor in children. Patients whose tumors exhibit overexpression or amplification of the MYC oncogene (c-MYC) usually have an extremely poor prognosis, but there are no animal models of this subtype of the disease. Here we show that cerebellar stem cells expressing Myc and mutant Trp53 (p53) generate aggressive tumors following orthotopic transplantation. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS4478
Platform:
GPL1261
19 Samples
Download data: CEL
Series
Accession:
GSE34126
ID:
200034126
3.
Full record GDS4478

MYC-driven medulloblastoma model

Analysis of Myc/DNp53-infected tumors derived from stem cells or progenitors, uninfected stem cells, and patched tumor cells. Cerebellar stem cells expressing Myc and mutant Trp53 generate tumors similar to MYC-driven medulloblastoma (MB). Results provide insight into transformation to MB tumor.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 4 cell type, 3 genotype/variation, 4 other sets
Platform:
GPL1261
Series:
GSE34126
19 Samples
Download data: CEL
4.

HDAC and NFκB antagonists synergistically inhibit growth and metastatic dissemination of MYC-driven medulloblastoma

(Submitter supplied) Aberrant oncogenic activation of MYC drives tumorigenesis in the most aggressive subset of medulloblastoma, the most common malignant brain tumor in childhood. Metastatic dissemination at diagnosis and at recurrence is commonly observed in MYC-driven medulloblastomas. Since these tumors display remarkable resistance to standard multimodal therapeutic approaches, epigenetic modulators commonly altered in these tumors are highly promising targets for novel therapeutic approaches. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
6 Samples
Download data: TXT
5.

Class I HDAC inhibition reduces DNA damage repair capacity of MYC-amplified medulloblastoma cells

(Submitter supplied) MYC-driven Group 3 medulloblastoma (MB) (subtype II) is a highly aggressive childhood brain tumor. Sensitivity of MYC-driven MBs to class I histone deacetylase inhibitors (HDACi) has been previously demonstrated in vitro and in vivo. We here characterize the transcriptional effects of class I HDAC inhibition in MYC-driven MB and explore beneficial drug combinations. MYC-amplified Group 3 MB cells (HD-MB03) were treated with class I HDACi entinostat. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
12 Samples
Download data: CEL
Series
Accession:
GSE232148
ID:
200232148
6.

Human neural stem cells transduced with oncogenic elements associated with aggressive medulloblastoma

(Submitter supplied) Human neural stem and progenitor cells transformed with c-MYC, dominant-negative p53, constitutively active AKT and hTERT formed tumors in mice that recapitulated Group 3 medulloblastoma in terms of pathology and expression profile
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13158
6 Samples
Download data: CEL
Series
Accession:
GSE77475
ID:
200077475
7.

HDACi and PLK1i synergize in MYC-amplified MB

(Submitter supplied) We and others have demonstrated that MYC-amplified medulloblastoma (MB) cells are susceptible towards treatment with class I histone deacetylase inhibitors (HDACi). However, single drug treatment with HDACi has shown limited clinical efficacy. We hypothesized that addition of a second compound acting synergistically with HDACi may enhance efficacy. Gene expression changes in HDACi entinostat-treated cells identified, the cell cycle protein PLK1 as a potential second target. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
12 Samples
Download data: CEL, TXT
Series
Accession:
GSE220748
ID:
200220748
8.

Cooperative Targets of Combined mTOR/HDAC Inhibition Promote MYC Degradation

(Submitter supplied) Cancer treatments often require combinations of molecularly targeted agents to be effective. mTORi (rapamycin) and HDACi (MS-275/entinostat) inhibitors have been shown to be effective in limiting tumor growth, and here we define part of the cooperative action of this drug combination. More than 60 human cancer cell lines responded synergistically (CI<1) when treated with this drug combination compared to single agents. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
17 Samples
Download data: CEL
Series
Accession:
GSE97985
ID:
200097985
9.

A macrophage autonomous α4β1integrin-Syk-Rac2 signaling axis controls macrophage differentiation, tumor growth and metastasis

(Submitter supplied) Macrophages, play an essential role in promoting tumor growth by affecting angiogenesis, immune suppression, invasion and metastasis. The signal transduction events within macrophages which encode the complex cascade of events required for tumor growth and polarization of macrophages are poorly understood. We have discovered an ECM dependent signaling pathway in macrophages that regulates M2 macrophage differentiation, tumor growth, invasion and metastasis. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
12 Samples
Download data: CEL
Series
Accession:
GSE41717
ID:
200041717
10.

mRNA Expression Profiling of pooled medulloblastoma samples

(Submitter supplied) mRNA expression analysis of 4 different pools of medulloblastoma samples with characteristic cytogenetic aberrations Keywords: Genetic modification
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10531
2 Samples
Download data: GPR, TXT
Series
Accession:
GSE22823
ID:
200022823
11.

Targeting the Phosphoinositide 3-Kinase p110α Isoform Impairs Cell Proliferation, Survival and Tumor Growth in Small Cell Lung Cancer

(Submitter supplied) Purpose: The phosphoinositide 3-kinase (PI3K) pathway is fundamental for cell proliferation and survival and is frequently altered and activated in neoplasia, including carcinomas of the lung. In this study we investigated the potential of targeting the catalytic class IA PI3K isoforms in small cell lung cancer (SCLC), which is the most aggressive of all lung cancer types. Experimental Design: The expression of PI3K isoforms in patient specimens was analyzed. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
9 Samples
Download data: CEL
Series
Accession:
GSE40564
ID:
200040564
12.

Reduced chromatin binding of MYC is a key effect of HDAC inhibition in MYC amplified meduloblastoma

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL570
28 Samples
Download data: BW, CEL, TXT
Series
Accession:
GSE143386
ID:
200143386
13.

Reduced chromatin binding of MYC is a key effect of HDAC inhibition in MYC amplified meduloblastoma [expression]

(Submitter supplied) MYC is a driver oncogene in many cancers. Inhibition of MYC promises high therapeutic potential, but specific MYC inhibitors remain unavailable for clinical use. Previous studies suggest that MYC amplified Medulloblastoma cells are vulnerable to HDAC inhibition. Using co-immunoprecipitation, mass spectrometry and ChIP-sequencing we show that HDAC2 is a cofactor of MYC in MYC amplified primary medulloblastoma and cell lines. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
6 Samples
Download data: CEL
Series
Accession:
GSE143384
ID:
200143384
14.

Reduced chromatin binding of MYC is a key effect of HDAC inhibition in MYC amplified meduloblastoma [RNA-seq]

(Submitter supplied) MYC is a driver oncogene in many cancers. Inhibition of MYC promises high therapeutic potential, but specific MYC inhibitors remain unavailable for clinical use. Previous studies suggest that MYC amplified Medulloblastoma cells are vulnerable to HDAC inhibition. Using co-immunoprecipitation, mass spectrometry and ChIP-sequencing we show that HDAC2 is a cofactor of MYC in MYC amplified primary medulloblastoma and cell lines. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
2 Samples
Download data: TXT
Series
Accession:
GSE143379
ID:
200143379
15.

Reduced chromatin binding of MYC is a key effect of HDAC inhibition in MYC amplified meduloblastoma [ChIP-seq]

(Submitter supplied) MYC is a driver oncogene in many cancers. Inhibition of MYC promises high therapeutic potential, but specific MYC inhibitors remain unavailable for clinical use. Previous studies suggest that MYC amplified Medulloblastoma cells are vulnerable to HDAC inhibition. Using co-immunoprecipitation, mass spectrometry and ChIP-sequencing we show that HDAC2 is a cofactor of MYC in MYC amplified primary medulloblastoma and cell lines. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
20 Samples
Download data: BW
Series
Accession:
GSE143376
ID:
200143376
16.

Histone Deacetylase Inhibitor prevents cell growth in Burkitt's lymphoma by regulating PI3K/Akt pathways and leading to up regulation of micro RNA-143, -145 and -101

(Submitter supplied) In this study we analyzed gene expression profiles in a well-characterized BL cell line upon treatment with HDACi combined with chemotherapy. The impact on gene expression regulation was broader when HDACi was combined with chemotherapy, than when either therapy was used alone. As expected, treatment interfered in the regulation of cell cycle progression and enhanced cell death. Noteworthy was the effect on members of p53 signaling pathway. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5386
Platform:
GPL4133
8 Samples
Download data: TXT
Series
Accession:
GSE48399
ID:
200048399
17.
Full record GDS5386

Histone deacetylase inhibitor and chemotherapy combined effect on Raji Burkitt's lymphoma cell line

Analysis of Raji Burkitt's lymphoma (BL) cell line treated with histone deacetylase inhibitor HDACi (sodium butyrate, NaB) or chemotherapy (VP-16) or both for 24 hours. Results provide insight into the molecular effects of combined HDACi/VP-16 therapy of this aggressive B-cell lymphoma.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 4 protocol sets
Platform:
GPL4133
Series:
GSE48399
8 Samples
Download data: TXT
DataSet
Accession:
GDS5386
ID:
5386
18.

Novel MYC-driven medulloblastoma models generated by CRISPR activation of endogenous Myc

(Submitter supplied) Myc-driven Group 3 (G3) medulloblastoma (MB) is the most aggressive tumor among the four subgroups classified by transcriptome, genomic landscape and clinical outcomes. Several successful mouse models have been developed to recapitulate G3 MB tumor development; however, all models currently used facilitate tumorigenesis by constitutive ectopic expression of exogenously regulated Myc randomly integrated in multiple events into the genome. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: BW
Series
Accession:
GSE102096
ID:
200102096
19.

Novel MYC-driven medulloblastoma models generated by CRISPR activation of endogenous Myc

(Submitter supplied) Myc-driven Group 3 medulloblastoma (MB) is the most aggressive tumor among the four subgroups classified by transcriptome, genomic landscape and clinical outcomes. So far in all available mouse Group 3 models, the constitutive ectopic Myc expression was under control of LTR element or other exogenous promoters within the vectors, which were randomly inserted into the genome with multiple copies. Here we are deploying nuclease deficient CRISPR/dCas9-based transactivator that is targeted to promoter DNA sequences by specific guide RNA to force the transcriptional activation of endogenous Myc in p53-/-;cdkn2c-/- neurospheres cells. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
14 Samples
Download data: CEL
Series
Accession:
GSE102037
ID:
200102037
20.

Genome-wide assessment of H4K20me1 chromatin profile in D458 shNull and shSETD8 medulloblastoma cells

(Submitter supplied) The goal of this study was to examine the H4K20me1 profile in medulloblastoma cells with wild type SETD8 or depleted SETD8.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
4 Samples
Download data: BEDGRAPH
Series
Accession:
GSE121556
ID:
200121556
Format
Items per page
Sort by

Send to:

Choose Destination

Supplemental Content

db=gds|term=|query=1|qty=3|blobid=MCID_6669c110bb845b085b7abd75|ismultiple=true|min_list=5|max_list=20|def_tree=20|def_list=|def_view=|url=/Taxonomy/backend/subset.cgi?|trace_url=/stat?
   Taxonomic Groups  [List]
Tree placeholder
    Top Organisms  [Tree]

Find related data

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center