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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from MLL-AF6 positive leukemia cells

ABSTRACT: The MLL gene on chromosome 11 fuses to the AF6 gene on chromosome 6 in a balanced chromosomal translocation that is characetristic of certain adult and pediatric human leukemias. We established a murine leukemia model of MLL-AF6 using the retroviral MLL-AF6 contruct in a bone marrow transplantation system. Leukemic bone marrow cells from a sacrificed moribund mouse were thawed and RNA was extracted using TRIZOL (Invitrogen) and purified further using the RNAeasy kit (Qiagen) under standard conditions and and hybridized onto Affymetrix arrays.

ORGANISM(S): Mus musculus

SUBMITTER: Amit Sinha

PROVIDER: E-GEOD-43067 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1l.

Deshpande Aniruddha J AJ Chen Liying L Fazio Maurizio M Sinha Amit U AU Bernt Kathrin M KM Bernt Kathrin M KM Banka Deepti D Dias Stuart S Chang Jenny J Olhava Edward J EJ Daigle Scott R SR Richon Victoria M VM Pollock Roy M RM Armstrong Scott A SA

Blood 20130129 13

The t(6;11)(q27;q23) is a recurrent chromosomal rearrangement that encodes the MLLAF6 fusion oncoprotein and is observed in patients with diverse hematologic malignancies. The presence of the t(6;11)(q27;q23) has been linked to poor overall survival in patients with AML. In this study, we demonstrate that MLL-AF6 requires continued activity of the histone-methyltransferase DOT1L to maintain expression of the MLL-AF6-driven oncogenic gene-expression program. Using gene-expression analysis and gen ...[more]

PMID: 23361907

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Expression data from a human MLL-AF6 positive AML cell line

Project description:The MLL gene on chromosome 11 fuses to the AF6 gene on chromosome 6 in a balanced chromosomal translocation that is characetristic of certain adult and pediatric human leukemias. We established a murine leukemia model of MLL-AF6 using the retroviral MLL-AF6 contruct in a bone marrow transplantation system. The ML2 human MLL-AF6 positive leukemia cell line was used for gene expression profiling to assess the transctiptional profile in MLL-AF6 leukemias. RNA was extracted from the ML2 cell line cultured under standard conditionswith TRIZOL (Invitrogen), purified using RNAeasy(Qiagen) and hybridized onto Affymetrix arrays.

2013-04-03 | E-GEOD-43068 | biostudies-arrayexpress

Expression data from MLL-AF6 positive leukemia cells

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Genome wide mapping of histone 3 lysine 79 dimethylation in MLL-AF6 murine leukemias

Project description:We report the genome wide distribution of H3K79 dimethylation in mouse MLL-AF6 positive leukemias to assess whether this epigenetic mark drives MLL-target gene expression. Examination of H3K79 dimethylation in bone marrow cells from sacrificed terminally ill MLL-AF6 positive leukemic mice. The retroviral MSCV-IRES-neo-MLL-AF6 construct was transduced into mouse bone marrow lineage negative Kit +, Sca + (LSK) cells and these cells were injected after G418 selection into irradiated syngenic mice to establish MLL-AF6 positive leukemias.

2013-04-03 | E-GEOD-43062 | biostudies-arrayexpress

The basic helix-loop-helix transcription factor SHARP1 is an oncogenic driver in MLL-AF6 Acute Myelogenous Leukemia

Project description:Acute Myeloid Leukemia (AML) with MLL gene rearrangements demonstrate unique gene expression profiles driven by MLL-fusion proteins. Here, we identify the circadian clock transcription factor SHARP1 as a novel oncogenic target in MLL-AF6 AML, which has the worst prognosis among all subtypes of MLL rearranged AMLs. SHARP1 is expressed solely in MLL-AF6 AML, and its expression is regulated directly by MLL-AF6 / DOT1L. Suppression of SHARP1 induces robust apoptosis of human MLL-AF6 AML cells. Genetic deletion in mice delays the development of leukemia and attenuated leukemia-initiating potential, while sparing normal hematopoiesis. Mechanistically, SHARP1 binds to transcriptionally active chromatin across the genome and activates genes critical for cell survival as well as key oncogenic targets of MLL-AF6. Our findings demonstrate the unique oncogenic role for SHARP1 in MLL-AF6 AML.

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Project description:The purpose of this study is to investigate the transcriptional programs as it relates to disease latency initiated by different MLL fusion proteins, including: MLL-AF1p, MLL-AF6, MLL-Gas7, MLL-AF9 and MLL-ENL. Leukemia cell lines were established by transforming kit+ mouse bone marrow cells with retroviruses coding MLL-AF1p, MLL-AF6, MLL-Gas7, MLL-AF9 or MLL-ENL. At early phase after the cell lines were established, cells growing at exponential phase (cell density at 0.5~1x106/ml) were harvested for RNA extraction and sequencing purpose. Sequencing is performed on total RNA isolated from mouse leukemia cell lines generated from kit+ mouse bone marrow cells transduced with various MLL fusion proteins and is compared to control total RNA isolated from kit+ mouse bone marrow cells.

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RNA-Seq of human AML samples, and human cells transformed with MLL-ENL or MLL-AF6

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2021-01-31 | E-MTAB-5501 | biostudies-arrayexpress

Runx1 deficiency effect on MLL-ENL cells

Project description:To identify the target genes of Runx1 in MLL fusion leukemia, we performed microarray analysis using control and Runx1-deficient MLL-ENL leukemia cells. Runx1 intact and excised bone marrow cells were transduced with MLL-ENL and transplanted into congenic mice. Leukemic cells were harvested from moribund mice, and gene expression was compared using 3 independent leukemia cells for each genotype.

2013-06-30 | E-GEOD-47402 | biostudies-arrayexpress

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