Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A Functional Role of OLIG2 in Tumor Heterogeneity of MYC-amplified Medulloblastoma

ABSTRACT: A Functional Role of OLIG2 in Tumor Heterogeneity of MYC-amplified Medulloblastoma

PROVIDER: PRJNA780565 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16952058.fastq.gz	Fastqsanger.gz
	SRR16952059.fastq.gz	Fastqsanger.gz
	SRR16952060.fastq.gz	Fastqsanger.gz
	SRR16952061.fastq.gz	Fastqsanger.gz
	SRR16952062.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

A Functional Role of OLIG2 in Tumor Heterogeneity of MYC-amplified Medulloblastoma

Project description:A Functional Role of OLIG2 in Tumor Heterogeneity of MYC-amplified Medulloblastoma

| PRJNA780320 | ENA

A Functional Role of OLIG2 in Tumor Heterogeneity of MYC-amplified Medulloblastoma

Project description:To study how radiation alters the different types of cells during tumor recurrence in high-risk MYC-amplified MB, we performed scRNA-seq using the 10X Genomics scRNA-seq platform to compare the primary untreated tumors, residual tumors immediately following radiotherapy, and the spontaneously recurrent tumors 7-8 weeks post-irradiation using OLIG2-high MB002 PDX. We found that:1, the variety of cell types demonstrated that the MYC-amplified MB PDX tumors were heterogenous communities, comprising diverse cell types in a broad range differentiation states and developmental trajectories, and included the host-derived cells of the tumor microenvironment; 2, Radiation-induced transient changes in cellular heterogeneity that resolved as tumor recurred; 3, Recurrent tumors showed global changes in gene expression compared to primary tumors

2021-11-20 | GSE188887 | GEO

A Functional Role of OLIG2 in Tumor Heterogeneity of MYC-amplified Medulloblastoma

Project description:The goal of this study was to compare gene expression profiles of MYC-amplified medulloblastoma tumors under three distinct conditions: primary tumors prior to radiation treatment, tumors derived from implanted radio-resistant tumor cells, and spontaneously recurring tumors several weeks post-irradiation. The purpose of this experiment was to identify the moleular pathways that are impacted during radiation and those which contribute to tumor recurrence. Unsupervised hierarchical cluster analysis revealed that the tumors which spontaneously recurred in vivo closely resembled the primary tumors. Tumors from implanted post-radiation neurospheres, however, had markedly different profiles. We identified 44 upregulated and 23 downregulated genes in the spontaneously recurred tumors compared to untreated primary tumors. Furthermore, we identified 817 upregulated and 509 downregulated genes in tumors derived from implanted post-radiation neurospheres compared to untreated primary tumors. Among these genes, 756 (57%) genes were also differentially expressed between tumors derived from implanted post-radiation neurospheres and spontaneously recurrent tumors. The downregulated pathways in tumors derived from implanted post-radiation neurospheres were associated with p53, cell cycle, DNA replication, and DNA damage, and the upregulated genes are involved in metabolic pathways. This study demonstrates that radiation resistant tumor cells exhibit differential gene expression post-irradiation and during tumor recurrence and provides a framework for the study of genetic pathways leading to tumor recurrence post-irradiation.

2021-11-16 | GSE188789 | GEO

Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma

Project description:Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma

| PRJNA887081 | ENA

Proteomic research on effect of EIF4A1 inhibition in MYC-amplified Group 3 medulloblastoma

Project description:As the most life-threatening subtype of pediatric medulloblastoma (MB), MYC-amplified Group 3 (G3) MB lacks effective and selective therapeutics. We tried to indirectly target MYC (oncogenic driver and cancer-dependent molecule) production via inhibiting translational machinery. Through multiple datasets analyses on components of eIF4F (eukaryotic translation initiation factor 4F) complex, we found that EIF4A1 (major component with RNA helicase activity) has relatively higher expression level and the closest positive correlation with MYC in G3-MB among normal control and other 3 subtypes (e.g., WNT, SHH and G4). Both in vitro and in vivo experiments with MYC-amplified G3-MB cell lines showed effective growth inhibition upon EIF4A1 knockout or inhibitor treatment. Further FACS analysis found decreased cell proliferation and enhanced apoptosis on EIF4A1 inhibitor treatment. To explore the mechanisms of EIF4A1 inhibition on arresting MYC-amplified G3-MB, we performed the whole proteome analyses on corresponding MB cells treated with EIF4A1 inhibitor.

2020-10-15 | PXD022014 |

Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma [EPIC]

Project description:Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma [EPIC]

| PRJNA887097 | ENA

Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma. [CRISPRseq]

Project description:Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma. [CRISPRseq]

| PRJNA887789 | ENA

Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma [RNA-seq]

Project description:Cancer-selective metabolic vulnerabilities in MYC-amplified medulloblastoma [RNA-seq]

| PRJNA887094 | ENA

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

Project description: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. The MYC-HDAC2 complex is bound to genes defining the MYC-dependent transcriptional profile. Class I HDAC inhibition leads to stabilization and reduced DNA binding of MYC protein inducing a down-regulation of MYC activated genes (MAGs) and up-regulation of MYC repressed genes (MRGs). MAGs and MRGs are characterized by opposing biological functions and distinct E-box distribution. We conclude that MYC and HDAC2 (class I) are localized in a complex in MYC amplified medulloblastoma and drive a MYC-specific transcriptional program, which is reversed by the class I HDAC inhibitor entinostat. Thus, the development of HDAC inhibitors for treatment of MYC amplified medulloblastoma should include HDAC2 in its profile in order to directly target MYC´s trans-activating and trans-repressing function.

2020-09-01 | GSE143384 | GEO

Effect of OLIG2 inhibition on medulloblastoma stem cells

Project description:To investigate the role2 in brain tissue and medulloblastoma stem cells, we inhibited OLIG2 using an inhibitor, CT-179.

2024-09-11 | GSE234105 | GEO