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Aberrant RNA expression and splicing in childhood ETV6/RUNX1 acute lymphoblastic leukemia

ABSTRACT: Aberrant RNA expression and splicing in childhood ETV6/RUNX1 acute lymphoblastic leukemia

PROVIDER: PRJNA432067 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6638963.fastq.gz	Fastqsanger.gz
	SRR6638964.fastq.gz	Fastqsanger.gz
	SRR6638965.fastq.gz	Fastqsanger.gz
	SRR6638966.fastq.gz	Fastqsanger.gz

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Aberrant RNA expression and splicing in childhood ETV6/RUNX1 acute lymphoblastic leukemia

Project description:ETV6/RUNX1 E/R -positive acute lymphoblastic leukemia (ALL), as one of the most common childhood malignancies, its pathogenesis and mechanism remain to be elucidated comprehensively. Global gene expression profiling can provide insight into the underlying pathophysiology of disease processes. In this study we sought to gain further insight into the molecular mechanisms underlying E/R-positive ALL by examining transcriptional profiles of E/R-positive ALL patients. We investigated the Bone marrow transcriptional profiles of E/R-positive ALL patients. Bioinformatic and statistical methods, including differential expression analysis, lncRNA analysis, alternative splicing analysis and metabolic network analysis, were used to characterize the underlying molecular mechanisms for E/R-positive ALL.

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Project description:ETV6-RUNX1 is a first-hit mutation in childhood B cell precursor acute lymphoblastic leukaemia. ETV6-RUNX1 is a fusion protein which inherits the DNA-binding runt domain from RUNX1. Here we performed chromatin precipitation for native RUNX1 and ETV6-RUNX1 using RUNX1 antibodies and specifically for the ETV6-RUNX1 fusion using a V5-tag pull down.

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Project description:Acute lymphoblastic leukemia (ALL), the most common malignant disorder in childhood, is typically associated with numerical chromosomal aberrations, fusion genes or small focal deletions, thought to represent important pathogenetic events in the development of the leukemia. Mutations, such as single nucleotide changes, have also been reported in childhood ALL, but these have only been studied by sequencing a small number of candidate genes. Herein, we report the first unbiased sequencing of the whole exome of two cases of pediatric ALL carrying the ETV6/RUNX1 (TEL/AML1) fusion gene (the most common genetic subtype) and corresponding normal samples. A total of 14 somatic mutations were identified, including four and seven protein-altering nucleotide substitutions in each ALL. Twelve mutations (86%) occurred in genes previously described to be mutated in other types of cancer, but none was found to be recurrent in an extended series of 29 ETV6/RUNX1-positive ALLs. The number of single nucleotide mutations was similar to the number of copy number alterations as detected by single nucleotide polymorphism arrays. Although the true pathogenetic significance of the mutations must await future functional evaluations, this study provides a first estimate of the mutational burden at the genetic level of t(12;21)-positive childhood ALL. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from 2 leukemic bone marrow samples and two corresponding normal blood samples.

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