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Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature

ABSTRACT: Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature

PROVIDER: PRJNA272423 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1752200.fastq.gz	Fastqsanger.gz
	SRR1752210.fastq.gz	Fastqsanger.gz
	SRR1752201.fastq.gz	Fastqsanger.gz
	SRR1752211.fastq.gz	Fastqsanger.gz
	SRR1752202.fastq.gz	Fastqsanger.gz

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Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [Methylation]

Project description:We performed genome-wide DNaseI hypersensitive site in FLT3-ITD and WT patient samples. We report corresponding gene expression, promoter methylation patterns of differential DHSs as well as differentially occupied TF binding motifs using surrounding DNAseI cut profiles. We examined association patterns of FLT3 ITD and WT AMLs and found that FLT3-ITD signaling is associated with common gene expression and chromatin signature. Examination of DNA methylation patterns in FLT3 ITD and WT AML via microarray study.

2015-07-03 | E-GEOD-64934 | biostudies-arrayexpress

Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [Agilent]

Project description:We performed genome-wide DNaseI hypersensitive site in FLT3-ITD and WT patient samples. We report corresponding gene expression, promoter methylation patterns of differential DHSs as well as differentially occupied TF binding motifs using surrounding DNAseI cut profiles. We examined association patterns of FLT3 ITD and WT AMLs and found that FLT3-ITD signaling is associated with common gene expression and chromatin signature. Examination of gene expression patterns in FLT3 ITD and WT AML via microarray study.

2015-07-03 | E-GEOD-64873 | biostudies-arrayexpress

Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [Methylation]

2015-07-03 | GSE64934 | GEO

Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [Agilent]

2015-07-03 | GSE64873 | GEO

Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [ChIP-Seq]

2015-07-03 | E-GEOD-64862 | biostudies-arrayexpress

Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [DNAse-Seq]

Project description:We performed genome-wide DNaseI hypersensitive site in FLT3-ITD and WT patient samples. We report corresponding gene expression, promoter methylation patterns of differential DHSs as well as differentially occupied TF binding motifs using surrounding DNAseI cut profiles. We examined association patterns of FLT3 ITD and WT AMLs and found that FLT3-ITD signaling is associated with common gene expression and chromatin signature. Examination of genome-wide DNaseI hypersensitivite sites in FLT3 ITD and WT AML.

2015-07-03 | E-GEOD-64864 | biostudies-arrayexpress

Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [ChIP-Seq]

2015-07-03 | GSE64862 | GEO

Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [DNAse-Seq]

2015-07-03 | GSE64864 | GEO

Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature

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

2015-07-03 | GSE64874 | GEO

Chronic FLT3-ITD Signaling in Acute Myeloid Leukemia Is Connected to a Specific Chromatin Signature.

Project description:Acute myeloid leukemia (AML) is characterized by recurrent mutations that affect the epigenetic regulatory machinery and signaling molecules, leading to a block in hematopoietic differentiation. Constitutive signaling from mutated growth factor receptors is a major driver of leukemic growth, but how aberrant signaling affects the epigenome in AML is less understood. Furthermore, AML cells undergo extensive clonal evolution, and the mutations in signaling genes are often secondary events. To elucidate how chronic growth factor signaling alters the transcriptional network in AML, we performed a system-wide multi-omics study of primary cells from patients suffering from AML with internal tandem duplications in the FLT3 transmembrane domain (FLT3-ITD). This strategy revealed cooperation between the MAP kinase (MAPK) inducible transcription factor AP-1 and RUNX1 as a major driver of a common, FLT3-ITD-specific gene expression and chromatin signature, demonstrating a major impact of MAPK signaling pathways in shaping the epigenome of FLT3-ITD AML.

| S-EPMC4726916 | biostudies-literature

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