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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNA Seq of mouse leukemic cell lines harboring a homozygous Cyclin C knock-out and wild type controls

ABSTRACT: This experiment was perfomed to understand the role of Cyclin C in BCR-ABL1 driven leukemia. Bone marrow from mice harbouring a homozygous Cyclin C knock-out as well as from wild type control mice was transduced with a BCR-ABL1 expressing retrovirus to generate stable cell lines. Cells were harvested for RNA seq from in-vitro cultures of these cell lines (\\"in-vitro\\" samples). 500000 cells of the same cultures were injected into the tail vains of NSG mice. After 10 days the cells were isolated from the bone marrow of the recipient mice and collected for RNA sequencing (\\"ex-vivo\\" samples). Library prep and sequencing was perfomed for in-vitro and ex-vivo samples together.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Mus musculus

SUBMITTER: Thorsten Klampfl

PROVIDER: E-MTAB-13728 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

SFPQ-ABL1 and BCR-ABL1 utilise different signalling networks to drive B-cell acute lymphoblastic leukaemia

Project description:Philadelphia-like (Ph-like) acute lymphoblastic leukaemia (ALL) is a high-risk subtype of B-cell ALL characterised by a gene expression profile resembling Philadelphia Chromosome positive ALL (Ph+ ALL) in the absence of BCR-ABL1. Tyrosine kinase activating fusions, some involving ABL1, are recurrent drivers of Ph-like ALL and are targetable with tyrosine kinase inhibitors (TKIs). We identified a rare instance of SFPQ-ABL1 in a child with Ph-like ALL. SFPQ-ABL1 expressed in cytokine-dependent cell lines was sufficient to transform cells which were sensitive to ABL1-targeting TKIs. In contrast to BCR-ABL1, SFPQ-ABL1 localised to the nuclear compartment and was a weaker driver of cellular proliferation. Phosphoproteomics analysis showed upregulation of cell cycle, DNA replication and spliceosome pathways, and downregulation of signal transduction pathways, including ErbB, NF-kappa B, VEGF, and MAPK signalling in SFPQ-ABL1-, compared to BCR-ABL1-expressing cells. SFPQ-ABL1 expression did not activate PI3K/AKT signalling and was associated with phosphorylation of G2/M cell cycle proteins. SFPQ-ABL1 was sensitive to navitoclax and S-63845 and promotes cell survival through upregulation of Mcl-1 and Bcl-xL. SFPQ-ABL1 has functionally distinct mechanisms by which it drives ALL, including subcellular localisation, proliferative capacity, and activation of cellular pathways, highlighting the role that fusion partners have in mediating the function of ABL1 fusions.

2022-05-20 | PXD028925 | Pride

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2010-05-27 | E-GEOD-20987 | biostudies-arrayexpress

Retroviral transduction of CD34+ cells with P190 and P210 BCR/ABL1 fusion genes

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2009-05-12 | GSE16042 | GEO

Comparison of copy number variations between wildtype and BCL6 knockout BCR-ABL1-driven acute lymphoblastic leukemia

Project description:This comparative genomic hybridization (CGH) study investigated the effect of BCL6 on clonal evolution in BCR-ABL1-driven acute lymphoblastic leukemia (ALL). The frequencies of copy number alterations in BCR-ABL1-transformed BCL6+/+ and BCL6-/- leukemias were determined. Three BCR-ABL1-transformed BCL6+/+ and BCL6-/- ALL samples derived from mice were maintained for 4 month in cell culture and were subjected to CGH analysis. As control samples, normal untransformed splenoytes were used.

2010-09-29 | E-GEOD-24400 | biostudies-arrayexpress

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2022-05-17 | GSE202658 | GEO

SHP2 Is Required for BCR-ABL1-Induced Hematologic Neoplasms

Project description:BCR-ABL1-targeting tyrosine kinase inhibitors (TKIs) have revolutionized treatment of Philadelphia chromosome-positive (Ph+) hematologic neoplasms. Nevertheless, acquired TKI resistance remains a major problem in chronic myeloid leukemia (CML), and TKIs are less effective against Ph+ B-cell acute lymphoblastic leukemia (B-ALL). GAB2, a scaffolding adaptor that binds and activates SHP2, is essential for leukemogenesis by BCR-ABL1, and a GAB2 mutant lacking SHP2 binding cannot mediate leukemogenesis. Using a genetic loss-of-function approach and bone marrow transplantation (BMT) models for CML and BCR-ABL1+ B-ALL, we show that SHP2 is required for BCR-ABL1-evoked myeloid and lymphoid neoplasia. Ptpn11 deletion impairs initiation and maintenance of CML-like myeloproliferative neoplasm, and compromises induction of BCR-ABL1+ B-ALL. SHP2, and specifically, its SH2 domains, PTP activity and C-terminal tyrosines, is essential for BCR-ABL1+, but not WT, pre-B cell proliferation. The MEK/ERK pathway is regulated by SHP2 in WT and BCR-ABL1+ pre-B cells, but is only required for the proliferation of BCR-ABL1+ cells. SHP2 is required for SRC family kinase (SFK) activation only in BCR-ABL1+ pre-B cells. RNAseq reveals distinct SHP2-dependent transcriptional programs in BCR-ABL1+ and WT pre-B cells. Our results suggest that SHP2, via SFKs and ERK, represses MXD3/4 to facilitate a MYC-dependent proliferation program in BCR-ABL1-transformed pre-B cells.

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Project description:In order to investigate the function of MYC in ALL, we isolated bone marrow cells from conditional MYC knockout mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with CRE or empty vector control.

2013-07-11 | GSE30928 | GEO

Gene expression data of BCR-ABL1 transformed B cell precursors from Dusp6 wild-type and Dusp6 knockout mice

Project description:To elucidate the mechanism of Dusp6-mediated pre-B cell survival signaling, we investigated the gene expression pattern in BCR-ABL1-transformed Dusp6+/+ and Dusp6-/- B cell precursors. BCR-ABL1 transformed B cell precursors of Dusp6 wildtype and Dusp6 knockout mice were subjected to RNA isolation

2013-06-03 | E-GEOD-34832 | biostudies-arrayexpress

Gene expression data of BCR-ABL1 transformed B cell precursors from ETV5 wild-type and ETV5 knockout mice

Project description:To elucidate the mechanism of ETV5-mediated pre-B cell survival signaling, we investigated the gene expression pattern in BCR-ABL1-transformed ETV5+/+ and ETV5-/- B cell precursors. BCR-ABL1 transformed B cell precursors of ETV5wild-type and ETV5 knockout mice were subjected to RNA isolation

2013-06-03 | E-GEOD-34833 | biostudies-arrayexpress

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