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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Human RNA-seq]

ABSTRACT: Purpose: To characterize transcriptional changes associated with inhibition of Dot1l in 2 inv(16) patient AML samples Methods: We sequenced mRNA from patient samples that were exposed to 5 uM EPZ004777 or DMSO control for 7 days. Results: Inhibition of Dot1l leads to gene expression changes in genes related to cell growth and cell cycle. Examination of mRNA levels between cells treated with 5 uM EPZ004777 or DMSO control

ORGANISM(S): Homo sapiens

SUBMITTER: Tobias Neff

PROVIDER: E-GEOD-76747 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Human ChIP-seq]

Project description:Purpose: To characterize the genome-wide distribution of H3K79me2 in human leukemia cell lines treated with the Dot1l inhibitor EPZ004777 or control Methods: We performed Chip-seq for the H3K79me2 on the leukemia cell lines Mutz3, Loucy and Molm14 after 6 days in culture in the presence of 3uM EPZ004777 or DMSO control Results: H3K79me2 is completely erased from key target genes such as the HOXA cluster. Conclusions: Exposure of Mutz3, Loucy and Molm14 to 3uM EPZ004777 erases H3K79 methylation globally as well as on key loci ChIP-Seq for H3K79me2 on human leukemia cell lines exposed for 6 days to the Dot1l inhibitor EPZ004777

2016-01-12 | E-GEOD-76745 | biostudies-arrayexpress

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Mouse Dot1l ko RNA-seq]

Project description:Purpose: To characterize transcriptional changes associated with homozygous inactivation of Dot1l or Mll1 in MN1 driven AML Methods: We sequenced mRNA from murine LSK-cells transformed using forced expression of MN1 (MSCV-MN1-IRES-GFP), and transduced with Cre-vector to inactivate either Dot1l or Mll1. Cells were sorted for Cre-expression (pTomato fluorescent marker) or expression of an inert control vector. Results: Inactivation of either Dot1l or Mll1 in this model leads to a substantial delay or complete abrogation of leukemia development. Loss of Dot1l or Mll1 are associated with gene expression changes that have substantial overlap. In addition, genes that are downregulated follwing inactivation of Dot1l or Mll1 have substantial overlap with the gene set upregulated in MN1 transduced CMPs. Conclusions: MN1 mediated leukemogenesis is associated with a gene expression program that dependes on Mll1 and Dot1l Examination of mRNA levels between Dot1l f/f and Dot1l ko, and Mll1 f/f and Mll1 ko.

2016-01-12 | E-GEOD-76748 | biostudies-arrayexpress

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Mouse Mll1 ko RNA-seq]

Project description:Purpose: To characterize transcriptional changes associated with homozygous inactivation of Dot1l or Mll1 in MN1 driven AML Methods: We sequenced mRNA from murine LSK-cells transformed using forced expression of MN1 (MSCV-MN1-IRES-GFP), and transduced with Cre-vector to inactivate either Dot1l or Mll1. Cells were sorted for Cre-expression (pTomato fluorescent marker) or expression of an inert control vector. Results: Inactivation of either Dot1l or Mll1 in this model leads to a substantial delay or complete abrogation of leukemia development.Loss of Dot1l or Mll1 are associated with gene expression changes that have substantial overlap. In addition, genes that are downregulated follwing inactivation of Dot1l or Mll1 have substantial overlap with the gene set upregulated in MN1 transduced CMPs. Conclusions: MN1 mediated leukemogenesis is associated with a gene expression program that dependes on Mll1 and Dot1l Examination of mRNA levels between Dot1l f/f and Dot1l ko, and Mll1 f/f and Mll1 ko.

2016-01-12 | E-GEOD-76749 | biostudies-arrayexpress

Expression Profiling of Mixed Lineage Leukemia Cells Treated with a Potent Small-Molecule DOT1L Inhibitor

Project description:Cell lines bearing MLL translocations (MV4-11 and MOLM-13) were treated with a potent, selective inhibitor of the DOT1L histone methyl transferase. Treatment of MLL-rearranged cell lines with the DOT1L inhibitor selectively inhibits H3K79 methylation and blocks expression of leukemogenic genes. Here we provide expression profiling data of cells treated with DOT1L inhibitor or vehicle control. MV4-11 cells were treated with 3 uM EPZ004777 (DOT1L inhibitor) or vehicle control (0.1% DMSO) for 2, 4 and 6 days. MOLM-13 cells were treated with 3 uM EPZ004777 (DOT1L inhibitor) or vehicle control (0.1% DMSO) for 6 days. For each unique conditon, 3 biological replicates were generated for expression profiling.

2011-07-11 | E-GEOD-29828 | biostudies-arrayexpress

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Human RNA-seq]

Project description:Purpose: To characterize transcriptional changes associated with inhibition of Dot1l in 2 inv(16) patient AML samples Methods: We sequenced mRNA from patient samples that were exposed to 5 uM EPZ004777 or DMSO control for 7 days. Results: Inhibition of Dot1l leads to gene expression changes in genes related to cell growth and cell cycle.

2016-01-12 | GSE76747 | GEO

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Mouse ChIP-seq]

Project description:Purpose: To characterize the genome-wide distribution of H3K79me2 in murine MN1 driven myeloid leukemia Methods: We performed Chip-seq for the H3K79me2 in leukemias isolated from moribund mice that had been injected with common myeloid progenitors (CMPs) transduced with MSCV-MN1-GFP Results: H3K79me2 is enriched at key loci that 1. are bound by MN1 in the data set of Heuser et al, (Cancer Cell. 2011 Jul 12;20(1):39-52.), 2. upregulated upon transduction with MN1, and lose expression upon deletion of the H3K79 methyltransferase Dot1l. Conclusions: A leukemogenic program in MN1 leukemias is marked by H3K79me2 and dependent on this mark ChIP-Seq for H3K79me2 using MN1 driven leukemias isolated from the bone marrow of moribund mice.

2016-01-12 | E-GEOD-76746 | 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

Expression profiling of MDA-MB-231 breast cancer cells treated with DOT1L inhibitors and siDOT1L

Project description:MDA-MB-231 cell line with relatively high DOT1L levels was treated with two potent, selective inhibitors of the DOT1L histone methyl transferase. These compounds can inhibit cells migration and invasion and induce differentiation. Here we provide expression profiling data of cells treated with two DOT1L inhibitors [1] [2], DOT1L siRNA (siDOT1L) or control. MDA-MB-231 cells were treated with 1uM compound [1], 5uM compound [1], 2uM compound [2], 10 uM compound [2] (DOT1L inhibitors) or control (0.1% DMSO) for 14 days, or siDOT1L for 7 days. For each unique condition, 2 biological replicates were generated for expression profiling. Compound [1]: EPZ004777 (in Diagle et al., 2011) Compound [2]: Compound 55 (in Anglin et al., 2012)

2015-02-18 | E-GEOD-56630 | biostudies-arrayexpress

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Human ChIP-seq]

2016-01-12 | GSE76745 | 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

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