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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE54793 | GEO | 2014/02/08

SECONDARY ACCESSION(S): PRJNA237656

REPOSITORIES: GEO

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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

Mus musculus

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

| PRJNA237656 | ENA

Identification of negative feedback regulators in response to acute activation of BCR-ABL1 kinase signaling in MLL-AF4 and E2A-PBX1 acute lymphoblastic leukemia

Project description:Human B cell lineage acute lymphoblastic leukemia (ALL) cells carrying MLL-AF4 (SEM; BEL) and E2A-PBX1 (697) gene rearrangements were transduced with the mouse ecotropic receptor to permit subsequent entry of retroviral BCR-ABL1 GFP and GFP empty vectors (EV) pseudotyped with murine ecotropic envelope. GFP expression was measured by flow cytometry. Transductions with BCR-ABL1 GFP and GFP empty vectors (EV) were performed in the presence and absence of 2 mmol/l Imatinib (TKI). Washout of Imatinib in one series of experiments is indicated with an arrow. To study gene expression changes in MLL-AF4 and E2A-PBX1 B cell lineage ALL cells that were transduced with empty vectors (EV), BCR-ABL1 GFP in the presence of Imatinib (BCR-ABL1 OFF), washout of Imatinib (BCR-ABL1 ON) and subsequent re-addition of Imatinib, microarray analyses were performed.

2015-12-29 | GSE40836 | GEO

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.

2013-07-11 | GSE30889 | GEO

IKZF1 in BCR-ABL1 driven pre-B cells

Project description:In order to investigate the function of IKZF1 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 IKZF1-GFP or empty vector control (GFP) and subjected to gene expression analysis.

2013-11-22 | GSE30860 | GEO

Role and function of STAT5 in BCR-ABL1 driven pre-B cells

Project description:In order to investigate the function of STAT5 in ALL, we isolated bone marrow cells from STAT5 fl/fl mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with CRE-GFP or empty vector control (GFP) and subjected to gene expression analysis.

2011-08-24 | GSE24814 | GEO

Effects of Blnk reconstitution in BCR-ABL1 driven pre-B cells

Project description:In order to investigate the function of the adapterprotein Blnk in ALL, we isolated bone marrow cells from Blnk KO mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with Blnk-GFP or empty vector control (GFP) and subjected to gene expression analysis.

2013-10-31 | GSE31108 | GEO

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

2013-07-11 | E-GEOD-30889 | biostudies-arrayexpress

CGH data from AID WT vs AID KO BCR-ABL1 mouse leukemia cells

Project description:Activation-induced cytidine deaminase (AID) specific amplifications and deletions in BCR-ABL1 positive Leukemia mouse cells. Bone marrow from Balb/CJ WT and Balb/CJ AID KO mice was transduced with BCR-ABL1. The AID specific amplifications and deletions where analyzed with an Agilent 244A mouse whole Genome CGH Array.

2009-08-15 | GSE15093 | GEO

Role and function of STAT5 in BCR-ABL1 driven pre-B cells

2011-08-23 | E-GEOD-24814 | biostudies-arrayexpress

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