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Gene regulation in t(6 9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis [DNase-hypersensitivity]

ABSTRACT: Gene regulation in t(6 9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis [DNase-hypersensitivity]

PROVIDER: PRJNA1003073 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25557647.fastq.gz	Fastqsanger.gz
	SRR25557648.fastq.gz	Fastqsanger.gz
	SRR27329324.fastq.gz	Fastqsanger.gz

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Gene regulation in t(6;9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis [DNase-hypersensitivity]

Project description:Acute Myeloid Leukemia (AML) represents a heterogeneous group of hematological malignancies. The t(6;9)(p23;q34) translocation, giving rise to the DEK::NUP214 fusion protein, is a rare mutation which produces a highly aggressive AML associated with extremely poor prognosis. Here, we utilise genome-wide chromatin accessibility to elucidate how a normal gene regulatory networks is disrupted by DEK::NUP214. We find that DEK::NUP214 AML forms a specific GRN related to that of mutant NPM1 AML, but also displays an elevated leukemic stem cell signature, suggesting both similar and unique therapeutic vulnerabilities.

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Gene regulation in t(6 9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis

Project description:Gene regulation in t(6 9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis

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Gene regulation in t(6 9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis [RNA-seq]

Project description:Gene regulation in t(6 9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis [RNA-seq]

| PRJNA1003070 | ENA

Gene regulation in t(6;9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis [RNA-seq]

2024-01-04 | GSE240267 | GEO

Gene regulation in t(6;9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-01-04 | GSE240272 | GEO

The Epigenetic Regulator Landscape of HOX/MEIS Expression in AML [scRNA-seq]

Project description:Aberrant and constitutive activation of the clustered homeobox (HOX) genes and the three-amino-acid loop extension (TALE) domain-containing HOX co-factor MEIS1 (henceforth termed HOX/MEIS) is a recurrent feature in several types of myeloid and lymphoid leukemias. HOX/MEIS misexpression is linked to aberrant self-renewal and therapy resistance in leukemia, but the therapeutic targeting of this important pathway has remained elusive. Using AF10-rearranged leukemia as a prototypical example of HOX/MEIS dysregulation, we sought to comprehensively characterize chromatin regulators that sustain aberrant expression of these genes. We deployed a GFP-MEIS1 knock-in reporter cell line to conduct small-molecule inhibitor screens and a high-density domain-focused CRISPR-Cas9 screen targeting epigenetic regulators. We identified members of at least six distinct chromatin-modifying complexes as HOX/MEIS regulators, including previously characterized HOX/MEIS regulators such as DOT1L, AF10, ENL, and HBO1 as well as less well-characterized and completely novel HOX/MEIS regulators including AFF2, JADE3, casein kinase 2 and the chromatin reader SGF29. These HOX/MEIS regulators were important for the growth of AML cell lines representing diverse leukemia subtypes characterized by HOX/MEIS dysregulation including leukemias with AF10 rearrangements, MLL rearrangements, and NPM1 mutation. Determination of gene expression changes after perturbing each of these MEIS1 regulators in parallel using CROP-seq demonstrated that the deletion of DOT1L, ENL, AFF2, or SGF29 led to the downregulation of several genes associated with stem cell self-renewal and upregulation of differentiation-associated genes.

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Epigenetic regulator landscape of HOX/MEIS expression in AML

Project description:Epigenetic regulator landscape of HOX/MEIS expression in AML

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Gene regulation in t(6;9) DEK::NUP214 Acute Myeloid Leukemia resembles that of FLT3-ITD/NPM1 Acute Myeloid Leukemia but with an altered HOX/MEIS axis.

Project description: Not available

| S-EPMC10844093 | biostudies-literature

The Epigenetic Regulator Landscape of HOX/MEIS Expression in AML [scRNA-seq]

Project description:The Epigenetic Regulator Landscape of HOX/MEIS Expression in AML [scRNA-seq]

| PRJNA900364 | ENA

MEIS homeodomain proteins facilitate PARP1/ARTD1-mediated eviction of histone H1

Project description:Pre–B-cell leukemia homeobox (PBX) and myeloid ecotropic viral integration site (MEIS) proteins control cell fate decisions in many physiological and pathophysiological contexts, but how these proteins function mechanistically remains poorly defined. Focusing on the first hours of neuronal differentiation of adult subventricular zone–derived stem/progenitor cells, we describe a sequence of events by which PBX-MEIS facilitates chromatin accessibility of transcriptionally inactive genes: In undifferentiated cells, PBX1 is bound to the H1-compacted promoter/proximal enhancer of the neuron-specific gene doublecortin (Dcx). Once differentiation is induced, MEIS associates with chromatin-bound PBX1, recruits PARP1/ARTD1, and initiates PARP1-mediated eviction of H1 from the chromatin fiber. These results for the first time link MEIS proteins to PARP-regulated chromatin dynamics and provide a mechanistic basis to explain the profound cellular changes elicited by these proteins.

2017-07-21 | PXD007078 | Pride

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