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Gene expression analysis of Early immature and Late mature T-ALL cell lines

ABSTRACT: Early immature T-cell acute lymphoblastic leukemias (T-ALLs) account for about 5-10% of pediatric T-ALLs and are associated with poor prognosis. However, the genetic defects that drive the biology of these tumors remain largely unknown. Analysis of microarray gene expression signatures in adult T-ALL demonstrated a high prevalence of early immature leukemias and revealed a close relationship between these tumors and myeloid leukemias. Consistently, adult immature T- ALLs showed characteristic mutations in myeloid specific oncogenes and tumor suppressors including IDH1, IDH2, DNMT3A, FLT3 and NRAS. Moreover, we identified ETV6 mutations as a novel genetic lesion uniquely present in immature adult T-ALL. All together, our results demonstrate that early immature adult T- ALL represents a heterogeneous category of leukemias characterized by the presence of overlapping myeloid and T-ALL characteristics and highlight the role of ETV6 mutations in these tumors.

ORGANISM(S): Homo sapiens

PROVIDER: GSE48046 | GEO | 2013/06/18

SECONDARY ACCESSION(S): PRJNA208786

REPOSITORIES: GEO

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Gene expression analysis of Early immature and Late mature T-ALL cell lines

Project description:Early immature T-cell acute lymphoblastic leukemias (T-ALLs) account for about 5-10% of pediatric T-ALLs and are associated with poor prognosis. However, the genetic defects that drive the biology of these tumors remain largely unknown. Analysis of microarray gene expression signatures in adult T-ALL demonstrated a high prevalence of early immature leukemias and revealed a close relationship between these tumors and myeloid leukemias. Consistently, adult immature T- ALLs showed characteristic mutations in myeloid specific oncogenes and tumor suppressors including IDH1, IDH2, DNMT3A, FLT3 and NRAS. Moreover, we identified ETV6 mutations as a novel genetic lesion uniquely present in immature adult T-ALL. All together, our results demonstrate that early immature adult T- ALL represents a heterogeneous category of leukemias characterized by the presence of overlapping myeloid and T-ALL characteristics and highlight the role of ETV6 mutations in these tumors. Samples for microarray analysis were prepared and hybridized in Affymetrix Human U133 Plus 2.0 arrays according to the manufacturer’s instructions and as previously described. RNA was extracted from duplicate cultures of T-ALL cell lines treated for 24 h with vehicle. Interarray intensity differences were normalized with GCRMA.

2013-06-18 | E-GEOD-48046 | biostudies-arrayexpress

Gene Expression Profile of 57 human T-ALL samples collected in human clinical trial E2993 (Marks et al., 2009)

Project description:Analysis of microarray gene expression signatures in adult T-ALL demonstrated a high prevalence of early immature leukemias and revealed a close relationship between these tumors and myeloid leukemias. 57 adult T-ALL samples were analyzed

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Gene Expression Analyisis of T-ALL LOUCY cell lines treated with ETV6 siRNA vs. scramble control siRNA

Project description:Transcriptional effects of ETV6 inactivation in immature T-ALL were investigated by gene expression analysis upon siRNA-mediated knockdown of ETV6 in LOUCY cells, a T-ALL cell line with a transcriptional program highly related to that of immature T-ALLs. Gene Set Enrichment Analysis (GSEA) of the ETV6 knockdown signature showed a significant enrichment in genes characteristically upregulated in ETV6 mutant immature T-ALLs including HOXA13, PRDM16, PTEN and CD33.

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Gene Expression Profile of 53 human T-ALL samples collected in human clinical trial E2993 (Marks et al., 2009)

Project description:To analyze the prognostic relevance of transcriptional profiling in adult T-ALL, we analyzed a clinical series of 53 primary leukemia samples uniformly treated according to the ECOG E2993 protocol using gene expression oligonucleotide microarrays. Unsupervised analysis and consensus clustering of microarray gene expression data in this series revealed the presence of 2 stable gene expression clusters corresponding to early immature (n = 28) and cortical/mature (n = 25) adult T-ALLs respectively. Early immature T-ALLs show a gene expression signature related to hematopoietic stem cells and myeloid progenitors that was recently linked to a group of childhood T-ALLs with poor prognosis. Notably, univariate analysis in our patient series confirmed that early immature adult T-ALL is associated with poor prognosis and reduced overall survival compared with cortical/mature adult T-ALL (P = 0.0197) 53 adult T-ALL samples were analyzed

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Gene Expression Analyisis of T-ALL LOUCY cell lines treated with ETV6 siRNA vs. scramble control siRNA

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Transcriptomic analysis of Acute Myeloid Leukemia and T Acute Lymphoblastic Leukemia

Project description:Diagnostic classification of Acute Myeloid and Lymphoid Leukemias (AMLs and ALLs) is mostly based on immunophenotype. This approach can pose challenges for phenotypically heterogeneous immature leukemias, and doesn't take account of recent advances in understanding of the developmental multipotency of diverse hematopoietic progenitor populations. We performed transcriptional analyses of a large series of primary ALs, including a high proportion of immature cases, in order to understand the spectrum of differentation arrest in AL. These transcriptional profiles were compared with both normal hematopoietic progenitors and independent leukemia data-sets.

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Project description:Mutations in the isocitrate dehydrogenase 1 (IDH1) and IDH2 genes are frequently observed in a wide variety of hematologic malignancies, including myeloid and T-cell leukemias. In this study, we generated Idh2R140Q transgenic mice to examine the role of the Idh2R140Q mutation in leukemia. No leukemia developed in Idh2R140Q transgenic mice, suggesting a need for additional genetic events for leukemia development. Since myeloid cells from NUP98-HOXD13 fusion (NHD13) transgenic mice frequently acquire somatic Idh mutations when they transform to AML, we generated Idh2R140Q/NHD13 double transgenic mice. Idh2R140Q/NHD13 transgenic mice developed an immature T cell leukemia with an immunophenotype similar to double-negative 1 (DN1) or DN2 thymocytes. Idh2R140Q/NHD13 leukemic cells were enriched for an early thymic precursor transcriptional signature, and the gene expression profile for Idh2R140Q/NHD13 DN1/DN2 T-ALL closely matched that of human early/immature T cell precursor (EITP) ALL. Moreover, recurrent mutations found in EITP ALL patients, including KRAS, PTPN11, JAK3, SH2B3, and EZH2 were also found in Idh2R140Q/NHD13 DN1/DN2 T-ALL. In vitro treatment of Idh2R140Q/NHD13 thymocytes with enasidenib, a selective inhibitor of mutant IDH2, led to a marked decrease in leukemic cell proliferation. These findings demonstrate that Idh2R140Q/NHD13 mice can serve as a useful in vivo model for the study of EITP ALL development and therapy. We used gene expression arrays to compare the global gene expression profiles between Idh2R140Q/NHD13 DN1/DN2 T-ALL, non-DN1/DN2 cortical T-ALL (CD4+CD8+) and wild-type thymus.

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Idh1-R132H mutation increases murine hematopoietic progenitors and alters epigenetics.

Project description:Mutations in the IDH1 and IDH2 genes encoding isocitrate dehydrogenases are frequent in human glioblastomas1 and cytogenetically normal acute myeloid leukemias (AML)2. These alterations are gain-of-function mutations in that they drive the synthesis of the M-bM-^@M-^\oncometaboliteM-bM-^@M-^] R-2-hydroxyglutarate (2HG)3. It remains unclear how IDH1 and IDH2 mutations modify myeloid cell development and promote leukemogenesis. Here we report the characterization of conditional knock-in mice in which the most common IDH1 mutation, Idh1-R132H, is inserted into the endogenous murine Idh1 locus and is expressed in cells of the hematopoietic (Vav-KI) or more specifically in cells of the myeloid (LysM-KI) lineage. These mutants show increased numbers of early hematopoietic progenitors and develop splenomegaly and anemia with extramedullary hematopoiesis, suggesting a dysfunctional bone marrow niche. Furthermore, LysM-KI cells exhibit both hypermethylated histones and changes to DNA methylation similar to those observed in human IDH1/2-mutant AML. Thus, our study is the first to describe the generation of conditional Idh1-R132H-KI mice. Furthermore, our study is also the first report showing the induction of a leukemic DNA methylation signature in a modeled system and sheds light on the mechanistic links between IDH1 mutation and human AML. DNA methylation profiling in LSK cells from IDH1-R132H knock-in mice vs. control mice

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