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MLL partner genes confer distinct biological and clinical signatures of pediatric AML, an AIEOP study

ABSTRACT: We retrospectively analyzed AML patients enrolled in the AIEOP since 2000, 42 patients with 11q23 rearrangement were analyzed by gene expression profile Gene expression analyses were performed to compare AML MLL partner genes (AF9, AF10, AF6, ENL, ELL, Septin 6, and AF1q) Keywords: Expression data Class comparison between different AML MLL partner genes

ORGANISM(S): Homo sapiens

SUBMITTER: Andrea Zangrando

PROVIDER: E-GEOD-19577 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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MLL partner genes drive distinct gene expression profiles and genomic alterations in pediatric acute myeloid leukemia: an AIEOP study.

Pigazzi M M Masetti R R Bresolin S S Beghin A A Di Meglio A A Gelain S S Trentin L L Baron E E Giordan M M Zangrando A A Buldini B B Leszl A A Putti M C MC Rizzari C C Locatelli F F Pession A A Te Kronnie G G Basso G G

Leukemia 20110218 3

PMID: 21331072

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MLL partner genes confer distinct biological and clinical signatures of pediatric AML, an AIEOP study

Project description:We retrospectively analyzed AML patients enrolled in the AIEOP since 2000, 42 patients with 11q23 rearrangement were analyzed by gene expression profile Gene expression analyses were performed to compare AML MLL partner genes (AF9, AF10, AF6, ENL, ELL, Septin 6, and AF1q) Keywords: Expression data

2011-04-21 | GSE19577 | GEO

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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Transcription profiling of human lymphoblastic and myeloblastic leukemia samples with and without MLL rearrangements specific and lineage specific signatures

Project description:Gene expression analysis identified a MLL translocation-specific signature of differentially expressed genes discriminating ALL and AML with and without MLL rearrangements. Gene expression signatures of acute lymphoblastic and myeloblastic leukemia samples with and without MLL rearrangements were analyzed using paired supervised analyses. Experiment Overall Design: ALL and AML patients with and without MLL rearrangements have been studied using paired class comparison (SAM) and class prediction (PAM) analyses.

2009-08-07 | E-GEOD-14062 | biostudies-arrayexpress

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

Project description:RNA-Seq of 1) human AML samples; 2) sorted, uncultured distinct population from human cord blood (CB); 3) short-term (ST) cultured sorted CB cells transduced with MLL-ENL, MLL-AF6 or untransduced; and 4) cultured (LT) sorted CB cells transformed with MLL-ENL or MLL-AF6. Cells from MLL-fusion AML patients are bulk. Several cords were used for the sorting (CB1, CB2, CB3, 135, 141...) and these represent biological replicates. Several samples were sequenced several times in different lanes and results were merged together for the analysis (rep1,rep2...). Samples were used to determine the different effect of MLL-fusions in different celltypes just after the transduction, and after a longer time period when cells were transformed. Sorted CB samples, uncultured as well as transformed by MLL-fusions, were used in machine learning approach to predict which of the patients originated from which cell-type of origin.

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

Homo sapiens

Project description:MLL partner genes confer distinct biological and clinical signatures of pediatric AML, an AIEOP study

| PRJNA122467 | ENA

Progenitor like cell type of an MLL-EDC4 fusion in acute myeloid leukemia

Project description:Transcriptome analysis by single cell sequencing provides valuable information on intratumor heterogeneity and developmental stages of acute myeloid leukemia (AML) as well as interactions of tumor cells with the microenvironment. However, it has been hardly applied to the subgroup of cases with translocations of the mixed lineage leukemia (MLL) gene for which the enhancer of mRNA decapping 4 (EDC4) gene was recently identified as a novel fusion partner (MLL-EDC4). Here, we compared different MLL translocation by single cell RNA sequencing of cells derived from peripheral blood. The AML MLL-EDC4 patient almost exclusively showed a transcriptional profile of hematopoietic progenitor cells while leukemic cells while the MLLT3-MLL and MLL-ELL fusions exhibited a more differentiated phenotype. The MLL-EDC4 progenitor state was characterized by the upregulation of key transcriptional regulators in AML (RUNX1, SOX4, HOPX), target genes of MYC and interferon signaling as well as other genes known to play a critical role in hematopoiesis or leukemic stem cell activation (CDK6, FLT3, NPM1). In addition, we detected an enrichment of a normal and putatively immunosuppressive monocyte population in the patient with MLL-EDC4. Thus, the MLL-EDC4 translocation was associated with unique transcriptional and microenvironmental features.

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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.

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Expression data from MLL-AF6 positive leukemia cells

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

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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.

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