Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tumor suppressor role of Ezh2 in an NRASQ61K driven model of Early T-cell Precursor Acute Lymphoblastic Leukemia

ABSTRACT: Tumor suppressor role of Ezh2 in an NRASQ61K driven model of Early T-cell Precursor Acute Lymphoblastic Leukemia

PROVIDER: PRJNA308125 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR3088870.fastq.gz	Fastqsanger.gz
	SRR3088871.fastq.gz	Fastqsanger.gz
	SRR3088872.fastq.gz	Fastqsanger.gz
	SRR3088855.fastq.gz	Fastqsanger.gz
	SRR3088856.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Tumor suppressor role of Ezh2 in an NRASQ61K driven model of Early T-cell Precursor Acute Lymphoblastic Leukemia (RNA-Seq)

Project description:Purpose: To characterize transcriptional changes associated with homozygous inactivation the Polycomb Repressive Complex 2 (PRC2) lysine methyltransferase Ezh2 in a mouse model of earlt T-cell precursor ALL (ETP-ALL) Methods: We sequenced mRNA from NRASQ61K transformed murine LSK-cells co-transduced with a self-inactivating Cre-vector. Cells were sorted for Cre-expression (lox-stop-loxRosa26-YFP) or expression of an inert control vector (GFP) and differentiated on OP9DL1 stroma with and without a functional Ezh2 gene. Results: Inactivation of Ezh2 in this model leads to accelerated leukemia development. Resulting gene expression changes are complex and include enrichment of genes associated with immature hematopoietic cells, Ras signaling and Cytokines and their cognate receptors. Conclusions: Inactivation of Ezh2 in our model leads to accentuated expression of early hematopoietic gene expression programs and to accentuated growth and survival signaling. Examination of mRNA levels between Ezh2ff and Ezh2ko in vivo, Ezh2ff and Ezh2ko in vitro.

2016-01-07 | E-GEOD-76602 | biostudies-arrayexpress

Tumor suppressor role of Ezh2 in an NRASQ61K driven model of Early T-cell Precursor Acute Lymphoblastic Leukemia (ChIP-Seq)

Project description:Purpose: To characterize changes in genome-wide H3K27me3 associated with homozygous inactivation the Polycomb Repressive Complex 2 (PRC2) lysine methyltransferase Ezh2 in a mouse model of earlt T-cell precursor ALL (ETP-ALL) Methods: We performed Chip-seq for the H3K27me3 Chromatin mark on Ezh2ff and Ezh2ko cells NRASQ61K leukemias. Results: Inactivation of Ezh2 in this model leads to accelerated leukemia development. Resulting gene expression changes are complex and include enrichment of genes associated with immature hematopoietic cells, Ras signaling and Cytokines and their cognate receptors. Genes that lose K27me3 in Ezh2ko vs. Ezh2ff cells (ChIP-Seq) are enriched by GSEA in Ezh2ko vs Ezh2ff cells. Conclusions: Inactivation of Ezh2 in our model leads to accentuated expression of early hematopoietic gene expression programs, to accentuated growth and survival signaling and to transcriptonal enrichment of PRC2 targets. ChIP-Seq for H3K27me3 using Ezh2ff and Ezh2ko NRASQ61K leukemias harvested from leukemic mice and expanded on OP9DL1 cells.

2016-01-07 | E-GEOD-76601 | biostudies-arrayexpress

Tumor suppressor role of Ezh2 in an NRASQ61K driven model of Early T-cell Precursor Acute Lymphoblastic Leukemia (RNA-Seq)

2016-01-07 | GSE76602 | GEO

Tumor suppressor role of Ezh2 in an NRASQ61K driven model of Early T-cell Precursor Acute Lymphoblastic Leukemia (ChIP-Seq)

2016-01-07 | GSE76601 | GEO

Unique long non-coding RNA expression signature in ETV6/RUNX1-driven B-cell precursor acute lymphoblastic leukemia

Project description:Unique long non-coding RNA expression signature in ETV6/RUNX1-driven B-cell precursor acute lymphoblastic leukemia

| PRJNA317293 | ENA

Tumor suppressor role of Ezh2 in an NRASQ61K driven model of Early T-cell Precursor Acute Lymphoblastic Leukemia

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-01-07 | E-GEOD-76603 | biostudies-arrayexpress

The tumor suppressor gene rap1GAP is silenced by mir-101-mediated EZH2 overexpression in invasive squamous cell carcinoma

Project description:Rap1GAP is a critical tumor suppressor gene that is down-regulated in multiple aggressive cancers such as head and neck squamous cell carcinoma, melanoma and pancreatic cancer. However, the mechanistic basis of rap1GAP down-regulation in cancers is poorly understood. By employing an integrative approach, we demonstrate polycomb-mediated repression of rap1GAP that involves EZH2, a histone methyltransferase in head and neck cancers. We further concomitant down-regulation of rap1GAP in head and neck cancers. EZH2 represses rap1GAP by facilitating the trimethylation of H3K27, a mark of gene repression, and also hypermethylation of rap1GAP promoter. These results provide a conceptual framework involving a microRNA-oncogene-tumor suppressor axis to understand head and neck cancer progression. OSCC3-siRNA Non-Targeting Vs. siRNA EZH2 with dye-swap, HOK-Adeno CMV Vs. Adeno EZH2.

2011-11-02 | E-GEOD-28501 | biostudies-arrayexpress

Human B-cell precursor acute lymphoblastic leukemia cells overexpressing ST6Gal1

Project description:Human B-cell precursor acute lymphoblastic leukemia cells overexpressing ST6Gal1

| PRJNA770077 | ENA

Lnc-RNA expression pattern in ETV6/RUNX1-driven b-cell precursor acute lymphoblastic leukemia (BCP-ALL)

Project description:Overwhelming evidence indicates that long non-coding RNAs have essential roles in tumorigenesis. Nevertheless, their expression and role in pediatric B-cell precursor acute lymphoblastic leukemia has not been extensively explored. Here, we conducted a comprehensive analysis of the long non-coding RNA transcriptome in ETV6/RUNX1 positive BCP-ALL, one of the most frequent subtypes of pediatric leukemia. An ETV6/RUNX1 expression signature was established, consisting of 596 lncRNAs (434 up and 162 down) using expression analysis of a series of primary patient samples. Subsequently, RNA sequencing from BCP-ALL cell lines and shRNA-mediated silencing of ETV6/RUNX1, illustrated that lnc-NKX2-3-1, lnc-TIMM21-5, lnc-ASTN1-1 and lnc-RTN4R-1 are bona fide ETV6/RUNX1 targets and could serve as novel biomarkers of this prevalent subtype of human leukemia.

2016-09-26 | GSE79869 | GEO

Transcription profiling of human T-cell acute lymphoblastic leukemia, T-cell lymphoblastic lymphoma and B-precursor acute lymphoblastic leukemia samples

Project description:T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LL) and are often thought to represent a spectrum of a single disease. The malignant cells in T-ALL and T-LL are morphologically indistinguishable, and they share the expression of common cell surface antigens and cytogenetic characteristics. However, despite these similarities, differences in the predominant sites of disease in T-ALL and T-LL are observed. To determine if underlying biological distinctions may potentially contribute to some of these differences, we analyzed the global gene expression profiles of malignant T-cell precursors in ten T-ALL and nine T-LL using DNA arrays. Ten additional B-precursor ALL bone marrow samples, were used in a separate analysis. <br><br> Note that files GSM27087.txt and GSM27088.txt are identical as downloaded from GEO.

2007-08-13 | E-GEOD-1577 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data