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Refining the set of ETV6-RUNX1-specific genes by employing gene expression profiles of patients in remission

ABSTRACT: The chromosomal translocation t(12;21) resulting in the ETV6-RUNX1 fusion gene is the most common genetic abnormality in childhood acute lymphoblastic leukemia (ALL). As the emergence of microarray technology, finding subtype-specific genes becomes one of the main objectives in most ALL studies. However, the list of differentiated genes derived by comparing patients in the subtype versus the others contains many false positives, which are not really subtype-specific. In order to refine the list of subtype-specific genes for ALL with ETV6-RUNX1, this study conducted microarray experiments on patients in both diagnosis and remission status.

ORGANISM(S): Homo sapiens

PROVIDER: GSE74335 | GEO | 2019/02/01

REPOSITORIES: GEO

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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.

2022-04-01 | GSE176084 | GEO

Identification of ETV6/RUNX1 regulated lncRNAs

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.

2016-09-26 | GSE79868 | GEO

Genome wide mapping of ETV6 binding sites in pre-B leukemic cells

Project description:Background: Genetic alterations in the transcriptional repressor ETV6 are associated with hematological malignancies. Notably, the t(12;21) translocation leading to an ETV6-AML1 fusion gene is the most common genetic alteration found in childhood acute lymphoblastic leukemia. Moreover, most of these patients also lack ETV6 expression, suggesting a tumor suppressor function. Results: To gain insights on ETV6 DNA-binding specificity and genome wide transcriptional regulation capacities, we performed chromatin immunoprecipitation experiments coupled to deep sequencing in a t(12;21)-positive pre-B leukemic cell line. This strategy led to high quality ETV6-bound regions. ETV6 binding is mostly cell type-specific as only few regions are shared with other blood cell subtypes. Peaks localization and motif enrichment analyses revealed a unique binding profile that is associated with the presence of the ETV6-AML1 fusion product. Conclusions: We described the first ETV6 binding map in the t(12;21) background. This study highlighted the complex and unique interplay between ETV6 and ETV6-AML1 and underscored the highly regulated mechanisms of ETV6 binding. ETV6 inactivation observed in this context could induce specific transcriptional changes promoting leukemic transformation.

2017-11-15 | GSE102785 | 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

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

Lnc-RNA expression pattern in ETV6/RUNX1-driven b-cell precursor acute lymphoblastic leukemia (BCP-ALL)

2016-09-26 | GSE79869 | GEO

Loss of BTG1 function promotes ETV6-RUNX1-mediated leukemic transformation by upregulation of BCL6

Project description:Analysis of gene signatures in WT+Ctrl vs WT+ETV6-RUNX1, Btg1-/- and Btg1-/-+ETV6-RUNX1 in cKit+Ter119- fetal liver-derived hematopoietic progenitor cells (FL-HPCs). The Btg1-/-+ETV6-RUNX1 FL-HPCs display a strong increase in proliferation compared to WT+ETV6-RUNX1. Total RNA otained from WT+Ctrl, WT+ETV6-RUNX1, Btg1-/-+Ctrl and Btg1-/-+ETV6-RUNX1 FL-HPCs cells that were cultured for 12 days in expansion medium.

2014-08-22 | E-GEOD-60589 | biostudies-arrayexpress

Loss of BTG1 function promotes ETV6-RUNX1-mediated leukemic transformation by upregulation of BCL6

2014-08-22 | GSE60589 | GEO

Loss of BTG1 function promotes ETV6-RUNX1-mediated leukemic transformation by upregulation of BCL6

2014-08-22 | GSE60589 | GEO

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

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