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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

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

ORGANISM(S): Mus musculus

SUBMITTER: Tobias Neff

PROVIDER: E-GEOD-76603 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2016-01-07 | GSE76603 | GEO

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)

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 (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

Ezh2 Controls an Early Hematopoietic Program and Growth and Survival Signaling in Early T Cell Precursor Acute Lymphoblastic Leukemia.

Project description: Not available

| S-EPMC4790111 | biostudies-literature

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

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

| PRJNA308125 | ENA

Early precursor T-cell acute lymphoblastic leukemia: current paradigms and evolving concepts.