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Infection exposure is a causal factor in B-precursor acute lymphoblastic leukemia as a result of Pax5 inherited susceptibility

ABSTRACT: We used microarrays to investigate gene expression changes in tumor-bearing Pax5+/- mice Tumor-bearing bone marrows of three Pax5+/- mice compared with B220+ bone marrow B cells from five WT mice

ORGANISM(S): Mus musculus

SUBMITTER: Isidro Sánchez García

PROVIDER: E-GEOD-62529 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Infection exposure is a causal factor in B-precursor acute lymphoblastic leukemia as a result of Pax5 inherited susceptibility

Project description:We used microarrays to investigate gene expression changes in tumor-bearing Pax5+/- mice

2014-10-21 | GSE62529 | GEO

Pax5 drives the metabolic shift in the development of pB-ALL as a result of BCR/ABLp190 susceptibility

Project description:We used microarrays to investigate gene expression changes in tumor-bearing Sca1-BCR/ABLp190 and Sca1-BCR/ABLp190+Pax5+/- mice. We also analyze gene expression changes in preleukemic Sca1-BCR/ABLp190 and Sca1-BCR/ABLp190+Pax5+/- mice

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Label free quantitativeproteomics of MDSCs

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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

Role and function of PAX5 in BCR-ABL1 driven pre-B cells

Project description:In order to investigate the function of PAX5 in ALL, we isolated bone marrow cells from C57Bl6 mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with PAX5-GFP or empty vector control (GFP) and subjected to gene expression analysis. Three days post transduction, total RNA of GFP positive sorted cells were extracted and subjected to gene expression analysis.

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Reduction in Pax5 activity drives ionizing radiation-mediated B-cell acute lymphoblastic leukemia development by modulating DNA-damage response

Project description:We used microarrays to investigate gene expression changes in tumor-bearing Pax5+/- IR and WT-IR mice. We also analyze gene expression changes in preleukemic Pax5+/- IR and WT-IR mice

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Ebf1 or Pax5 Haploinsufficiency Synergizes with STAT5 Activation to Initiate Acute Lymphoblastic Leukemia

Project description:STAT5 is critical for differentiation, proliferation and survival of progenitor B cells suggesting a possible role in Acute Lymphoblastic Leukemia (ALL). Herein, we show increased expression of activated STAT5 in ALL patients, which correlates with treatment outcome. Mutations in Ebf1 and Pax5, genes critical for B cell development have also been identified in human ALL. To determine whether mutations in Ebf1 or Pax5 synergize with STAT5 activation to induce ALL we crossed mice expressing a constitutively active form of STAT5 (Stat5b-CA) with mice heterozygous for Ebf1 or Pax5. Haploinsufficiency of either Pax5 or Ebf1 synergized with Stat5b-CA to rapidly induce ALL in 100% of the mice. The leukemic cells displayed reduced expression of both Pax5 and Ebf1 but this had little affect on most EBF1 or PAX5 target genes. However, a subset of these genes was deregulated and included a large percentage of potential tumor suppressor genes and oncogenes. Further, most of these genes appear to be jointly regulated by both EBF1 and PAX5. Our findings suggest a model whereby small perturbations in a self-reinforcing network of transcription factors critical for B cell development, specifically PAX5 and EBF1, cooperate with STAT5 activation to initiate ALL. Gene expression profiling was performed on cells isolated from lymph nodes of Stat5b-CA x Ebf1+/- and Stat5b-CA x Rag2-/- leukemic mice and pre B cells sorted from bone marrow of C57BL/6 mice and Stat5b-CA transgenic mice. 17 Samples.

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Role and function of PAX5 in BCR-ABL1 driven pre-B cells

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Molecular role of the PAX5-ETV6 oncoprotein in promoting B cell acute lymphoblastic leukemia

Project description:PAX5 is a tumor suppressor in B-ALL, while the role of PAX5 fusion proteins in B-ALL development is largely unknown. Here we studied the function of PAX5-ETV6 and PAX5- FOXP1 in mice expressing these proteins from the Pax5 locus. Both proteins arrested Blymphopoiesis at the pro-B-to-pre-B cell transition and, contrary to their proposed dominantnegative role, did not interfere with the expression of most Pax5 target genes. Pax5-Etv6, but not Pax5-Foxp1, cooperated with loss of the Cdkna2a/b tumor suppressor in promoting B-ALL development. Regulated Pax5-Etv6 target genes identified in these B-ALLs encode proteins implicated in pre-BCR signaling and migration/adhesion, which could contribute to the proliferation, survival and tissue infiltration of leukemic B-cells. Together with similar observations made in human PAX5-ETV6+ B-ALLs, these data identified PAX5-ETV6 as a potent oncoprotein. 36 samples in total: A) 24 RNA-Seq samples in 5 cell types: pro-B (5 genotypes, 2-4 replicates) large pre-B (2 genotypes, 2 replicates each) small pre-B (1 genotype, 2 replicates) lymph node (1 genotype, 3 replicates) bone marrow (1 genotype, 2 replicates) B) 12 ChIP-Seq samples in 2 cell types: pro-B (H3K27me3, H3K9ac, H3K4me2, H3K4me3, H3K27ac, 1 replicate each; Pax5Etv6 ChIP, Prd ChIP, 2 replicates each; Pax5 ChIP 1 replicate) lymph node (1 genotype, 2 replicates).

2016-07-30 | E-GEOD-84987 | biostudies-arrayexpress

RNAseq of pro-B cells and CD19+B220- cells in the bone marrow of WT and PAX5 Y351*/351* mice

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