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LMO2 expression in HSCs causes T-ALL in the presence of an intact thymic niche [preleukemic and leukemic cells]

ABSTRACT: We used microarrays to investigate gene expression changes in tumor-bearing Sca1-TOMATO-Lmo2 mice and in preleukemic cells from Sca1-TOMATO-Lmo2 mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE83570 | GEO | 2016/06/22

SECONDARY ACCESSION(S): PRJNA326407

REPOSITORIES: GEO

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LMO2 expression in HSCs causes T-ALL in the presence of an intact thymic niche [preleukemic and leukemic cells]

Project description:We used microarrays to investigate gene expression changes in tumor-bearing Sca1-TOMATO-Lmo2 mice and in preleukemic cells from Sca1-TOMATO-Lmo2 mice. Tumor-bearing thymus of eleven Sca1-TOMATO-Lmo2 mice compared with thymus cells from 4 WT mice, with TOMATO-positive thymus preleukemic T cells from 5 Sca1-TOMATO-Lmo2 mice and with TOMATO-negative thymus preleukemic T cells from 5 Sca1-TOMATO-Lmo2 mice GSM2209749 - GSM220975 and GSM2209757 - GSM2209759 were re-analyzed by GSE83571 (GSM2209767 - GSM2209776).

2016-06-22 | E-GEOD-83570 | biostudies-arrayexpress

LMO2 expression in HSCs causes T-ALL in the presence of an intact thymic niche [nude mice]

Project description:We used microarrays to investigate gene expression changes in tumor-bearing Sca1-TOMATO-Lmo2 Nu/Nu mice Tumor-bearing bone marrows of three Sca1-TOMATO-Lmo2 Nu/Nu mice compared with bone marrow cells from four Control Nude mice and with thymus leukemic cells from ten Sca1-TOMATO-Lmo2 mice. GSM2209767 - GSM2209776 are re-analyses of GSE83570 (GSM2209749 - GSM220975 and GSM2209757 - GSM2209759).

2016-06-22 | E-GEOD-83571 | biostudies-arrayexpress

LMO2 expression in HSCs causes T-ALL in the presence of an intact thymic niche [nude mice]

Project description:We used microarrays to investigate gene expression changes in tumor-bearing Sca1-TOMATO-Lmo2 Nu/Nu mice

2016-06-22 | GSE83571 | GEO

Impact of Lmo2 expression on cell lineage decision during T-cell leukemogenesis [RNA-seq]

Project description:The goal of this study is compare the transcriptome profilling of different genetically engineered mouse models to the Human scenerio, in order to better understand the role of Lmo2 expression on cell lineage decision during T-cell leukemogenesis. Results: The up-regulated Rosa26-Lmo2+Sca1-Cre and Sca1-Lmo2 signatures shows a significant enrichment in the human T-ALL group. Conclusion: The similarity between Rosa26-Lmo2+Sca1-Cre and Human T-ALL signature is in accordance to the Human T-ALL situation wherein the expression of LMO2 is present throughout in tumor cells.

2018-05-01 | GSE113864 | GEO

Lmo2 is dispensable for maintenance of most Lmo2-induced murine T-cell leukemias

Project description:Lmo2 is an oncogenic transcription factor that is a frequent target of chromosomal abnormalities in this T-cell acute lymphoblastic leukemia (T-ALL). In transgenic mouse models, overexpression of Lmo2 causes thymocyte self-renewal leading to T-cell leukemia with long latency. However, the requirement of Lmo2 for maintenance of overt leukemia is poorly understood. We found that Lyl1, a critical cofactor for Lmo2-induced leukemia, is frequently lost in cell lines derived from Lmo2-transgenic mice, raising the possibility that Lmo2 function is dispensable at this stage. To study this, we developed a Tetracycline-repressible knock-in mouse model (Vav-TRE-Lmo2), which expresses Lmo2 throughout the haematopoietic system. This led to specific effects on T-cell development and the development of T-cell leukemia with long latency, preceded by the presence of self-renewing T-cells in the thymus. Repression of Lmo2 overcame the Lmo2-induced thymocyte developmental block at the preleukemic stage and led to elimination of Lmo2-induced thymocyte self-renewal in vivo. In contrast, Lmo2 function was dispensable for the majority of overt Lmo2-induced T-cell leukemias as well as leukemia-derived cell lines, implying an evolution of oncogene addiction in the majority of T-cell leukemias. Lmo2-dependence in T-ALL was associated with an immature gene expression profile, but could not be predicted by immunophenotype or assessment of Notch pathway activation. Thus, Lmo2 can give rise to both Lmo2-depenent and –independent T-cell leukemias. The Vav-TRE-Lmo2 model should be useful to determine the molecular features associated with Lmo2-dependence, as well as the critical components of the Lmo2-induced self-renewal pathways in T-ALL.

2022-01-01 | GSE125674 | GEO

Loss of Ikaros promotes oncogene independence in a model of Lmo2-induced T-cell acute lymphoblastic leukemia

Project description:LMO2 is an oncogenic transcription factor that is frequently overexpressed due to chromosomal abnormalities in T-cell acute lymphoblastic leukemia (T-ALL). In transgenic mouse models, Lmo2 overexpression causes thymocyte self-renewal resulting in T-cell leukemia with long latency. However, the requirement for Lmo2 for leukemia maintenance is poorly understood. To study this, we developed a Tetracycline-regulated knock-in mouse model that reversibly expresses Lmo2 throughout the haematopoietic system. This led to a specific impairment of T-cell development and the development of self-renewing preleukemic stem cells (pre-LSCs) in the thymus, followed by the development of fully penetrant T-lymphoblastic leukemia resembling human T-ALL. In preleukemic mice, repression of Lmo2 overcame the LMO2-induced thymocyte developmental block, reversed Lmo2-induced gene expression changes and eliminated self-renewing pre-LSCs in vivo. In contrast, overt T-lymphoblastic leukemias arising in this model were either immature, Lmo2-dependent leukemias resembling human ETP-ALL, or mature leukemias which were Lmo2-independent. Genomic analyses identified frequent loss of tumour suppressor genes in Lmo2-independent T-ALLs. Deletion of one of these, Ikaros (Ikzf1), was sufficient to transform Lmo2-dependent tumours to Lmo2-independence. Together these results indicate an evolution of oncogene addiction in T-ALL and that loss of Ikaros can promote self-renewal of T-ALL lymphoblasts in the absence of initiating oncogenes.

2020-12-31 | GSE144035 | GEO

LMO2 expression in HSCs causes T-ALL in the presence of an intact thymic niche

Project description:LMO2 expression in HSCs causes T-ALL in the presence of an intact thymic niche

| PRJNA326395 | ENA

Effect of PML/RARA on the transcriptome of preleukemic early promyelocytes vs PML/RARA-Flt3ITD leukemic promyelocytes

Project description:Transcriptional profiling of murine cells expressing PML/RARA at the early promyelocyte stage (4 weeks old, preleukemic) and in full blown PML/RARA leukemia generated by transducing PML/RARA bone marrow with a Flt3-ITD retroviral vector Two-conditions experiment: preleukemic early promyelocytes vs leukemic promyelocytes

2015-07-15 | E-GEOD-59431 | biostudies-arrayexpress

LMO2 expression in HSCs causes T-ALL in the presence of an intact thymic niche

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-06-22 | E-GEOD-83572 | biostudies-arrayexpress

LMO2 expression in HSCs causes T-ALL in the presence of an intact thymic niche

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-06-22 | GSE83572 | GEO