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Characterization of mesenchymal stem cells in pre-B acute lymphoblastic leukemia

ABSTRACT: The way in which leukemia develops, progresses and responds to treatment is mediated largely by components of the bone marrow microenvironment (BMM). Increasing evidence shows that leukemic cells hijack the BMM, altering its functioning and establishing leukemia-supportive interactions with stromal and immune cells. While previous work has highlighted functional defects in the mesenchymal stem cell (MSC) population from the BMM of acute leukemias, a thorough characterization and molecular profiling of MSCs of pre-B cell acute lymphoblastic leukemia (B-ALL), the most common cancer in children, has not been conducted. Here, we investigated the transcriptome profiles of MSCs isolated from the BMM of an immunocompetent BCR-ABL1+ model of B-ALL.

ORGANISM(S): Mus musculus

PROVIDER: GSE208719 | GEO | 2023/01/31

REPOSITORIES: GEO

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proteomic analysis of leukocytes upon Plekhm1-KO

Project description:Leukemia cells instruct their surrounding bone marrow microenvironment (BMM) rendering it hospitable to leukemia cell survival. Conversely, how cells of the BMM influence leukemia progression is less well understood. Pleckstrin homology domain family M member 1 (PLEKHM1) serves as a hub between fusion and secretion of intracellular vesicles. Here, we performed TMT-based quantitative proteomics to investigate the proteome of BMM-derived leucocytesfrom mice lacking Plekhm1 compared to wild-type animals, which have been transplanted withBCR-ABL1-expressing bone marrow cells.

2023-01-16 | PXD027044 | Pride

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ZMYM2/FGFR1, BCR/FGFR1 or BCR/ABL1 in human cord blood CD34+ cells reveals similar but distinct gene expression profiles

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The Impact of T cell Immunity on Chemotherapy Response in Childhood Acute Lymphoblastic Leukemia

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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

Recruitment of BCL6 to target genes in Philadelphia chromosome positive acute lymphoblastic leukemia

Project description:The Philadelphia chromosome (Ph) encodes the oncogenic BCR-ABL1 tyrosine kinase, which defines a subset of acute lymphoblastic leukemia (ALL) with a particularly unfavorable prognosis. Tyrosine kinase inhibitors (TKI) are widely used to treat patients with leukemia driven by BCR-ABL1 and other oncogenic tyrosine kinases. In response to TKI-treatment, BCR-ABL1 ALL cells upregulate BCL6 protein levels by ~90-fold, i.e. to similar levels as in diffuse large B cell lymphoma (DLBCL) with BCL6 translocations. In this study, we used genome tiling arrays to identify BCL6 target genes with specific recruitment of BCL6.

2011-02-15 | GSE24404 | GEO

Inhibition of BCL6-dependent gene expression in Philadelphia chromosome positive acute lymphoblastic leukemia

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2011-03-01 | GSE24381 | GEO

Exploiting Temporal Collateral Sensitivity in Tumor Clonal Evolution

Project description:In this study, using a murine model of Ph+ acute lymphoblastic leukemia (Ph+ ALL), a combined pharmacological profile and drug selection experimental approach identified distinct stages of tumor clonal evolution with vulnerabilities to sets of small molecules. Through genotypic, phenotypic, signaling, and binding measurements, we identified the mutation V299L in the ABL1 kinase domain as mediator for an on-target ABL1 inhibition and hence the sensitization phenotype. To further rule out any off-target effects, we performed RNA-seq analysis of select derived cell lines. Variant calls suggest that although there were other mutations, the only mutation shared among cell lines with the sensitization phenotype and that went from 0% to 100% variant allele frequency was c.895G>C, leading to BCR-ABL1 V299L. In addition, transcriptional profile does not suggest functional changes in BCR-ABL1 V299L and WT cell lines. RNA-seq of parental murine Ph+ acute lymphoblastic leukemia (Ph+ ALL) cell line and derived cell lines (via dose escalating concentrations of dasatinib or DMSO vehicle control).

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