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ATAC-seq of Kasumi-7 acute lymphoblastic leukemia cell line harboring MEF2D-HNRNPUL1 fusion gene

ABSTRACT: ATAC-seq of Kasumi-7 acute lymphoblastic leukemia cell line harboring MEF2D-HNRNPUL1 fusion gene

PROVIDER: PRJEB35179 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3632896_1.fastq.gz	Fastqsanger.gz
	ERR3632896_2.fastq.gz	Fastqsanger.gz

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MEF2D-HNRNPUL1 ChIP-seq in a genome-edited Kasumi-7 cell line

Project description:Acute lymphoblastic leukemia harboring the fusion genes involving the MEF2D transcription factor (MEF2D-ALL) is associated with poor clinical outcomes. To explore binding sites in the genome in MEF2D-ALL, we genome-edited a MEF2D-ALL cell line Kasumi-7 so that the fusion is tagged with HA at the carboxyl-terminal and co-expressed with GFP. We used this cell line for ChIP-seq using anti-HA antibody. Pair-end reads for Input and HA ChIP DNA are provided.

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ATAC-seq of Kasumi-7 acute lymphoblastic leukemia cell line harboring MEF2D-HNRNPUL1 fusion gene

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MEF2D-HNRNPUL1 ChIP-seq in a genome-edited Kasumi-7 cell line

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Functional, structural, and molecular characterizations of the leukemogenic driver MEF2D-HNRNPUL1 fusion.

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Project description:Chromosomal rearrangements are initiating events in acute lymphoblastic leukemia (ALL). Here, using RNA-sequencing (RNAseq) of 560 ALL cases, we identify rearrangements between MEF2D (myocyte enhancer factor 2D) and five genes (BCL9, CSF1R, DAZAP1, HNRNPUL1 and SS18) in 22 B progenitor ALL (B-ALL) cases with a distinct gene expression profile, the most common of which is MEF2D-BCL9. Examination of an extended cohort of 1164 B-ALL cases identified 30 cases with MEF2D rearrangements which include an additional fusion partner, FOXJ2, thus MEF2D-rearranged cases comprise 5.3% of cases lacking recurring alterations. MEF2D-rearranged ALL is characterized by a distinct immunophenotype, DNA copy number alterations at the rearrangement sites, older diagnosis age, and poor outcome. The rearrangements result in enhanced MEF2D transcriptional activity, lymphoid transformation, activation of HDAC9 expression and sensitive to histone deacetylase inhibitors treatment. Thus, MEF2D-rearranged ALL represents a distinct form of high-risk leukemia, for which new therapeutic approaches should be considered.

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