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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.

2021-01-20 | GSE109807 | GEO

ChIP-seq for RUNX1 and ETV6-RUNX1 in an induced pluripotent stem cell model of ETV6-RUNX1 pre-leukaemia

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.

2022-10-31 | E-MTAB-12208 | biostudies-arrayexpress

Illumina and Affymetrix SNP-array data for 2 ETV6/RUNX1-positive Acute Lymphoblastic Leukemia samples and corresponding normal samples

Project description:This SuperSeries is composed of the following subset Series: GSE25102: Illumina SNP-array data for 2 ETV6/RUNX1-positive Acute Lymphoblastic Leukemia samples and corresponding normal samples GSE25116: Affymetrix SNP-array data for 2 ETV6/RUNX1-positive Acute Lymphoblastic Leukemia samples and corresponding normal samples Refer to individual Series

2012-07-02 | E-GEOD-25117 | biostudies-arrayexpress

Whole-genome mapping of ETV6-RUNX1 in pre-B lymphoblast models

Project description:Genome binding/occupancy profiling of ETS Variant Transcription Factor 6- Runt Related Transcription Factor 1 fusion protein (ETV6-RUNX1) in REH cells by high throughput sequencing. ETV6-RUNX1 is expressed in pediatric t(12;21) ETV6-RUNX1 B cell precursor acute lymphoblastic leukemia.

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Affymetrix SNP-array data for 2 ETV6/RUNX1-positive Acute Lymphoblastic Leukemia samples and corresponding normal samples

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.

2012-07-02 | E-GEOD-25116 | biostudies-arrayexpress

Single cell characterization of arrested B-lymphoid differentiation and leukemic cell states in ETV6-RUNX1-positive pediatric leukemia

Project description:Arrested bone marrow (BM) lymphoid cell differentiation underlies the emergence of the most common childhood cancer, acute lymphoblastic leukemia (ALL). Recurrent genetic lesions often directly involve transcription factors (TFs), such as ETV6 and RUNX1 found in the most common ALL translocation.

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Project description:Overwhelming evidence indicates that long non-coding RNAs have essential roles in tumorigenesis. Nevertheless, their expression and role in pediatric B-cell precursor acute lymphoblastic leukemia has not been extensively explored. Here, we conducted a comprehensive analysis of the long non-coding RNA transcriptome in ETV6/RUNX1 positive BCP-ALL, one of the most frequent subtypes of pediatric leukemia. An ETV6/RUNX1 expression signature was established, consisting of 596 lncRNAs (434 up and 162 down) using expression analysis of a series of primary patient samples. Subsequently, RNA sequencing from BCP-ALL cell lines and shRNA-mediated silencing of ETV6/RUNX1, illustrated that lnc-NKX2-3-1, lnc-TIMM21-5, lnc-ASTN1-1 and lnc-RTN4R-1 are bona fide ETV6/RUNX1 targets and could serve as novel biomarkers of this prevalent subtype of human leukemia.

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Identification of ETV6/RUNX1 regulated lncRNAs

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Illumina SNP-array data for 2 ETV6/RUNX1-positive Acute Lymphoblastic Leukemia samples and corresponding normal samples

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. Illumina SNP-array genotyping was performed according to the manufacturer's directions on DNA extracted from 2 leukemic bone marrow samples and two corresponding normal blood samples. The genotype data from the arrays were used for quality assesment of genotype data from high throughput sequencing.

2012-07-02 | E-GEOD-25102 | biostudies-arrayexpress

Histone H3, lysine 27 acetylation ChIP-seq in NALM6 expressing ETV6-RUNX1

Project description:ETV6-RUNX1 is a fusion protein bringing together almost the entire coding sequence of RUNX1, including the DNA binding runt domain, and the N-terminus of ETV6 which is known to include transcriptional repressors including histone deacetylation 3 (HDAC3). Here we perform ChIP-seq for the active chromatin mark H3K27ac in the NALM6 B-cell acute lymphoblastic leukaemia cell line expressing ETV6-RUNX1 or mutant derivatives of ETV6-RUNX1: Delta helix-loop-helix (dHLH) is a deletion of the pointed domain; R139G is a point mutation in the runt DNA-binding domain.

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