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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE83571 | GEO | 2016/06/22

SECONDARY ACCESSION(S): PRJNA326406

REPOSITORIES: GEO

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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 [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 [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.

2016-06-22 | GSE83570 | GEO

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

| PRJNA326395 | ENA

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 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

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

Human LMO2 binding protein LC-MSMS in U87MG(Glioblastoma cell)

Project description:To identify the binding partner of LMO2 for explanation of STAT3 signal-related protein in human glioblastoma

2022-08-11 | PXD028254 | Pride

Identification of LMO2 transcriptome and interactome in diffuse large B-cell lymphoma

Project description:LMO2 regulates gene expression facilitating the formation of multipartite DNA-binding complexes. In B cells, LMO2 is specifically up-regulated in the Germinal Center (GC) reaction and is expressed in GC-derived non-Hodgkin’s lymphomas. LMO2 is one of the most powerful prognostic indicators in DLBCL patients. However, its function in GC B cells and DLBCL is currently unknown. In the present study we characterized the LMO2 transcriptome and interactome in DLBCL cells. LMO2 regulates genes implicated in kinetochore function, chromosome assembly and mitosis. Overexpression of LMO2 in DLBCL cell lines results in centrosome amplification. In DLBCL, the LMO2 complex contains some of the traditional partners such as LDB1, E2A, HEB, Lyl1, ETO2 and SP1, but not TAL1 or GATA proteins. Furthermore, we identified novel LMO2 interacting partners: ELK1, NFATc1 and LEF-1 proteins. Reporter assays revealed that LMO2 increases transcriptional activity of NFATc1 and decreases transcriptional activity of LEF-1 proteins. Overall, our studies identified a novel LMO2 transcriptome and interactome in DLBCL and provide a platform for future elucidation of LMO2 function in GC B-cells and DLBCL pathogenesis.

2012-07-13 | GSE34576 | GEO

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