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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE85600 | GEO | 2016/08/16

SECONDARY ACCESSION(S): PRJNA338921

REPOSITORIES: GEO

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Loss of Pax5 Exploits Sca1-BCR-ABLp190 Susceptibility to Confer the Metabolic Shift Essential for pB-ALL.

Project description: Not available

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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.

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

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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 Tumor-bearing bone marrows of three Pax5+/- mice compared with B220+ bone marrow B cells from five WT mice

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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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BET inhibition targets ABC-DLBCL constitutive B-cell receptor signaling through PAX5

Project description:B-cell receptor (BCR) signaling is essential for the diffuse large B-cell lymphoma (DLBCL) subtype that originates from activated B-cells (ABC). ABC-DLBCL cells are sensitive to Bruton tyrosine kinase intervention. However, ABC-DLBCL patients had overall response rates of 33-37% for Bruton tyrosine kinase inhibitors, suggesting the evaluation of combination-based treatment for improved efficacy. We investigated the efficacy and mechanism of AZD5153 combined with the Bruton tyrosine kinase inhibitor acalabrutinib in ABC-DLBCL preclinical models. AZD5153 is a bivalent BET inhibitor that simultaneously engages the two bromodomains of BRD4. Adding AZD5153 to acalabrutinib demonstrated a combination benefit in ABC-DLBCL cell lines and PDX models. Differential expression analyses in treated tumors identified significant alterations of BCR, PAX5, RELB/alternative NFκB, and toll-like receptor/interferon signaling. PAX5 is a transcription factor for BCR signaling genes and may be critical to the perpetually active BCR signaling in ABC-DLBCL. We demonstrate that AZD5153 decreases PAX5 expression, while acalabrutinib disruption to BCR signaling inhibits PAX5 activation. Furthermore, several interferons were decreased by AZD5153 and acalabrutinib in tumors. Adding IFNß1 to cells in vitro restored PAX5 activation. Our results demonstrate AZD5153 enhances the efficacy of acalabrutinib through PAX5 and BCR mechanisms that are critical for ABC-DLBCL.

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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

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Germline Aberrations of PAX5 Cause Susceptibility to pre-B cell Acute Lymphoblastic Leukemia

Project description:A novel heterozygous germline variant, c.547G>A (p.Gly183Ser), in the paired box protein encoding gene, PAX5, was found to segregate with disease in two unrelated kindreds with autosomal dominant pre-B cell acute lymphoblastic leukemia (ALL). Leukemic cells from both families exhibited 9p deletion, with loss-of-heterozygosity and retention of the mutant PAX5 allele at 9p13. Two additional sporadic ALL cases with 9p loss demonstrated PAX5 Gly183 substitution in the leukemic cells. Functional and gene expression analysis of the PAX5 germline variants demonstrated reduced transcriptional activity. These data extend the role of PAX5 alterations in the pathogenesis of pre-B ALL, and implicate PAX5 in a novel syndrome of germline susceptibility to pre-B cell neoplasia. We analyzed 40 samples comprising sevenfold replicates of transductions with empty vector, wild type PAX5 and 4 mutant PAX5 constructs

2013-08-01 | E-GEOD-45260 | biostudies-arrayexpress

Germline Aberrations of PAX5 Cause Susceptibility to pre-B cell Acute Lymphoblastic Leukemia

Project description:A novel heterozygous germline variant, c.547G>A (p.Gly183Ser), in the paired box protein encoding gene, PAX5, was found to segregate with disease in two unrelated kindreds with autosomal dominant pre-B cell acute lymphoblastic leukemia (ALL). Leukemic cells from both families exhibited 9p deletion, with loss-of-heterozygosity and retention of the mutant PAX5 allele at 9p13. Two additional sporadic ALL cases with 9p loss demonstrated PAX5 Gly183 substitution in the leukemic cells. Functional and gene expression analysis of the PAX5 germline variants demonstrated reduced transcriptional activity. These data extend the role of PAX5 alterations in the pathogenesis of pre-B ALL, and implicate PAX5 in a novel syndrome of germline susceptibility to pre-B cell neoplasia. We analyzed 10 samples of J558 murine myeloma cells infected with MSCV-Puro-IRES-GFP (PIG) empty vector (EV; three independent replicates), MSCV-PIG Pax5 WT (WT; three independent replicates), and MSCV-PIG Pax5 G183S (Mut; four independent replicates). Cells were selected with puromycin after infection for 5-7 days, subsequently cells were sorted for GFP and IgM expression by FACS.

2014-04-06 | E-GEOD-45834 | biostudies-arrayexpress

gamma-catenin (junction plakoglobin, Jup) dependent signals mediate the progression of BCR-ABL1+ B-ALL

Project description:The BCR-ABL1 translocation product is the cause of Chronic Myeloid Leukemia (CML) and of a significant fraction of adult-onset B-Acute Lymphoblastic Leukemia (B-ALL) cases. Here we identify an essential role for gamma-catenin (junction plakoglobin) in B lineage restricted cells for the progression of B-ALL in a mouse model. The array analysis of preleukemic B cells aimed at identifying genes that explain the deficient B-ALL progression in the absence gamma-catenin. Total bone marrow cells from chimeric mice expressing or lacking gamma-catenin in the hematopoietic compartment were transduced with BCR-ABL1+ IRES GFP retrovirus before transplantation into lethally irradiated wild type recipients. Three weeks later, GFP+ (BCR-ABL1+) B220+ BP-1+ B cells were flow sorted from the bone marrow of preleukemic recipient mice. The analysis includes 3 replicates for gamma-catenin WT and 3 replicates for gamma-catenin KO BCR-ABL1+ BP1+ B cells.

2014-02-08 | E-GEOD-54793 | biostudies-arrayexpress

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