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Homo sapiens

ABSTRACT: Base-pair resolution DNA methylation sequencing reveals profoundly divergent epigenetic landscapes in Acute Myeloid Leukemia

PROVIDER: PRJNA160145 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR489509.fastq.gz	Fastqsanger.gz
	SRR489510.fastq.gz	Fastqsanger.gz
	SRR489511.fastq.gz	Fastqsanger.gz
	SRR489512.fastq.gz	Fastqsanger.gz
	SRR489513.fastq.gz	Fastqsanger.gz

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Base-pair resolution DNA methylation sequencing reveals profoundly divergent epigenetic landscapes in Acute Myeloid Leukemia

Project description:Here we used Illumina NGS for high-throughput profiling of the DNA methylome in two human colon cancer derived cell lines, two human normal bone marrow CD34+ controls and in five human Acutre Myeloid Leukeima patient samples. These data can be used to determine the CpG cytosine methylation pattern at base pair resolution in each sample and to determine differentially methylated cytosines and regions between samples Reduced Representation Bisulfite Sequencing (RRBS) and Extended Reduced Representation Bisulfite Sequencing (ERRBS) on genomic DNA. We used colon cancer cell lines (two) to establish reproducbility and range of assay sensitivity. We used Acute Myeloid Leukemia patient samples and CD34+ bone marrow cells as controls to determine the methylome pattern in the patient samples

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THP1 immunopeptidogenomics data

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Methylation profiling by array shows that mIDH-associated DNA hypermethylation in acute myeloid leukemia reflects differentiation blockage rather than inhibition of TET-mediated demethylation

Project description:Isocitrate dehydrogenases 1 and 2 (IDH1/2) are recurrently mutated in acute myeloid leukemia (AML), but their mechanistic role in leukemogenesis is poorly understood. The inhibition of TET enzymes by D-2-hydroxyglutarate (D-2-HG), which is produced by mutant IDH1/2 (mIDH1/2), has been suggested to promote epigenetic deregulation during tumorigenesis. In addition, mIDH also induces a differentiation block in various cell culture and mouse models. Here we analyze the genomic methylation patterns of AML patients with mIDH using Infinium 450K data from a large AML cohort and found that mIDH is associated with pronounced DNA hypermethylation at tens of thousands of CpGs. Interestingly, however, myeloid leukemia cells overexpressing mIDH, cells that were cultured in the presence of D-2-HG or TET2 mutant AML patients did not show similar methylation changes. In further analyses, we also characterized the methylation landscapes of myeloid progenitor cells and analyzed their relationship to mIDH-associated hypermethylation. Our findings identify the differentiation state of myeloid cells, rather than inhibition of TET-mediated DNA demethylation, as a major factor of mIDH-associated hypermethylation in AML. Furthermore, our results are also important for understanding the mode of action of currently developed mIDH inhibitors.

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