TEL-AML1 (ETV6-RUNX1) in B-cells and leukemia
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ABSTRACT:
PROVIDER: PRJNA218611 | ENA |
REPOSITORIES: ENA
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Project description:Around 20-25% of childhood acute lymphoblastic leukemias carry the TEL-AML1 (TA) fusion gene. It is a fusion of two central hematopoietic transcription factors, TEL (ETV6) and AML1 (RUNX1). Despite its prevalence, the exact genomic targets of TA have remained elusive. We evaluated gene loci and enhancers targeted by TA genome-wide in precursor B acute leukemia cells using global nuclear run-on sequencing (GRO-seq).
2015-12-31 | GSE67519 | GEO
Project description:Around 20-25% of childhood acute lymphoblastic leukemias carry the TEL-AML1 (TA) fusion gene. It is a fusion of two central hematopoietic transcription factors, TEL (ETV6) and AML1 (RUNX1). Despite its prevalence, the exact genomic targets of TA have remained elusive. We evaluated gene loci and enhancers targeted by TA genome-wide in precursor B acute leukemia cells using global nuclear run-on sequencing (GRO-seq). Nascent RNA expression profiles were generated with GRO-seq after TEL-AML1 expression in the Nalm6 pre-B-ALL cell line in four different time points (0, 4, 12 and 24 h). TEL-AML1-mut and luciferase induction cell lines were used as controls. Two replicates were included for all six samples.
2015-12-31 | E-GEOD-67519 | biostudies-arrayexpress
Project description:We identified directly and indirectly regulated target genes utilizing an inducible TEL-AML1 system derived from the murine pro B-cell line BA/F3 and a monoclonal antibody directed against TEL-AML1. By integration of promoter binding identified with ChIP-on-chip, gene expression and protein output through microarray technology and stable labelling of amino acids in cell culture (SILAC), we identified directly and indirectly regulated targets of the TEL-AML1 fusion protein.
2013-11-04 | GSE50734 | GEO
Project description:We identified directly and indirectly regulated target genes utilizing an inducible TEL-AML1 system derived from the murine pro B-cell line BA/F3 and a monoclonal antibody directed against TEL-AML1. By integration of promoter binding identified with ChIP-on-chip, gene expression and protein output through microarray technology and stable labelling of amino acids in cell culture (SILAC), we identified directly and indirectly regulated targets of the TEL-AML1 fusion protein.
2013-11-04 | GSE50733 | GEO
Project description:We identified directly and indirectly regulated target genes utilizing an inducible TEL-AML1 system derived from the murine pro B-cell line BA/F3 and a monoclonal antibody directed against TEL-AML1. By integration of promoter binding identified with ChIP-on-chip, gene expression and protein output through microarray technology and stable labelling of amino acids in cell culture (SILAC), we identified directly and indirectly regulated targets of the TEL-AML1 fusion protein.
2013-11-04 | GSE50732 | GEO
Project description:We identified directly and indirectly regulated target genes utilizing an inducible TEL-AML1 system derived from the murine pro B-cell line BA/F3 and a monoclonal antibody directed against TEL-AML1. By integration of promoter binding identified with ChIP-on-chip, gene expression and protein output through microarray technology and stable labelling of amino acids in cell culture (SILAC), we identified directly and indirectly regulated targets of the TEL-AML1 fusion protein.
2013-11-04 | GSE50731 | GEO
Project description:We identified directly and indirectly regulated target genes utilizing an inducible TEL-AML1 system derived from the murine pro B-cell line BA/F3 and a monoclonal antibody directed against TEL-AML1. By integration of promoter binding identified with ChIP-on-chip, gene expression and protein output through microarray technology and stable labelling of amino acids in cell culture (SILAC), we identified directly and indirectly regulated targets of the TEL-AML1 fusion protein.
2013-11-04 | GSE50730 | GEO
Project description:We identified directly and indirectly regulated target genes utilizing an inducible TEL-AML1 system derived from the murine pro B-cell line BA/F3 and a monoclonal antibody directed against TEL-AML1. By integration of promoter binding identified with ChIP-on-chip, gene expression and protein output through microarray technology and stable labelling of amino acids in cell culture (SILAC), we identified directly and indirectly regulated targets of the TEL-AML1 fusion protein.
2013-11-04 | GSE50735 | GEO
Project description:Background The t(12;21)(p13;q22) translocation is found in 20 to 25% of cases of childhood B-lineage acute lymphoblastic leukemia (B-ALL). This rearrangement results in the fusion of ETV6 (TEL) and RUNX1 (AML1) genes and defines a relatively uniform category, although only some patients suffer very late relapse. TEL/AML1-positive patients are thus an interesting subgroup to study, and such studies should elucidate the biological processes underlying TEL/AML1 pathogenesis. We report an analysis of gene expression in 60 children with B-lineage ALL using Agilent whole genome oligo-chips (44K-G4112A) and/or real time RT-PCR. Results We compared the leukemia cell gene expression profiles of 16 TEL/AML1-positive ALL patients to those of 44 TEL/AML1-negative patients, whose blast cells did not contain any additional recurrent translocation. Microarray analyses of 26 samples allowed the identification of genes differentially expressed between the TEL/AML1-positive and negative ALL groups. Gene enrichment analysis defined five enriched GO categories: cell differentiation, cell proliferation, apoptosis, cell motility and response to wounding, associated with 14 genes –RUNX1, TCFL5, TNFRSF7, CBFA2T3, CD9, SCARB1, TP53INP1, ACVR1C, PIK3C3, EGFL7, SEMA6A, CTGF, LSP1, TFPI— highlighting the biology of the TEL/AML1 sub-group. These results were first confirmed by the analysis of an additional microarray data-set (7 patient samples) and second by real-time RT-PCR quantification and clustering using an independent set (27 patient samples). Over-expression of RUNX1 (AML1) was further investigated and in one third of the patients correlated with cytogenetic findings. Conclusions Gene expression analyses of leukemia cells from 60 children with TEL/AML1-positive and -negative B-lineage ALL led to the identification of five biological processes, associated with 14 validated genes characterizing and highlighting the biology of the TEL/AML1-positive ALL sub-group. Keywords: Acute lymphoblastic leukemia, gene expression profiles, TEL/AML1 fusion transcript, functional annotation
2007-09-27 | GSE9170 | GEO
Project description:We identified directly and indirectly regulated target genes utilizing an inducible TEL-AML1 system derived from the murine pro B-cell line BA/F3 and a monoclonal antibody directed against TEL-AML1. By integration of promoter binding identified with ChIP-on-chip, gene expression and protein output through microarray technology and stable labelling of amino acids in cell culture (SILAC), we identified directly and indirectly regulated targets of the TEL-AML1 fusion protein. Bound promoter regions of immunoprecipitated TEL-AML1 associated genes were first compared to input material and enrichment was calculated. 3 independent replicates were performed.
2013-11-04 | E-GEOD-50733 | biostudies-arrayexpress