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Ena-DATASET-DCG-LU-16-05-2016-08:49:49:640-82 - samples

ABSTRACT: RNA-seq data from 195 pediatric BCP-ALL cases. Alignment: TopHat 2.0.7. Reference genome: hg19.

PROVIDER: EGAD00001002112 | EGA |

REPOSITORIES: EGA

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ena-DATASET-DCG-LU-16-05-2016-09:33:32:167-83 - samples

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Project description:Despite considerable improvements in the treatment of B-cell precursor acute lymphoblastic leukemia (BCP-ALL), relapse is still associated with poor prognosis. We previously found that the risk for early relapse can be predicted by the rapid engraftment of patient-derived blasts transplanted into NOD/SCID mice. In search for the cellular and molecular profile associated with this phenotype, we investigated the expression of microRNAs (miRNAs) in different engraftment phenotypes and patient outcomes. We found miR-497~195 high expression in patient-derived xenograft samples with slow engraftment, derived from patients with favorable outcome. In contrast, epigenetic repression and low expression of these miRNAs was observed in rapidly engrafting samples, which were associated with early relapse. Overexpression of miR-497~195 in patient-derived cells suppressed in vivo engraftment of leukemia cells and considerably prolonged recipient survival by inhibition of regulators of cell cycle progression. As key factors for the entry in S phase were downregulated upon miR-497~195 overexpression, we identified CDK4/CCND3 mediated control of G1/S transition as a principal mechanism for miR-497~195 mediated suppression of leukemia progression in BCP-ALL. Thus, the association of the miR-497~195 cluster expression with outcome in BCP-ALL, and the importance of these miRNAs in counteracting the development of ALL in vivo indicate the relevance of the involved pathways as potential targets for therapeutic intervention.

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The miR-497~195 cluster suppresses cell cycle regulators and in vivo leukemia growth in B-cell precursor Acute Lymphoblastic Leukemia [expression]

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Expression data from mesenchymal stromal cells derived from pediatric leukemia patients and healthy pediatric controls

Project description:B-cell precursor acute lymphoblastic leukemia (BCP-ALL) cells reside in the bone marrow microenvironment, where they are protected against chemotherapeutic agents. Mesenchymal stromal cells (MSCs) are key components of this supporting framework. The present study aimed to unravel whether MSCs derived from pediatric BCP-ALL patients (leukemic MSCs) differ from MSCs derived from healthy pediatric donors (control-MSCs). Therefore, we studied their gene expression profiles.

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Project description:Analysis of patient-derived xenograft cells at the basal level. A panel of T- and BCP-ALL pediatric leukaemia xenograft cells were utilised to further understand the biology of pediatric leukaemia. Total RNA were isolated from patient-derived xenograft cells. Illumina beadchip HT12 were utilised

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Repurposing CD19-directed immunotherapies for pediatric t(8;21) acute myeloid leukemia

Project description:In contrast to patients with B cell precursor acute lymphoblastic leukemia (BCP-ALL), patients with acute myeloid leukemia (AML) have not yet benefited from recent advances in targeted immunotherapy. Repurposing immunotherapies that have been successfully used to target other hematological malignancies could, in case of a shared target antigen, represent a promising opportunity to expand the immunotherapeutic options for AML. Here, we evaluated the expression of CD19 in a large pediatric AML cohort, assessed the ex vivo AML killing efficacy of CD19-directed immunotherapies, and characterized the bone marrow immune microenvironment in pediatric AML, BCP-ALL, and non-leukemic controls. Out of 167 newly diagnosed de novo pediatric AML patients, 18 patients (11%) had CD19+ AML, with 61% carrying the translocation t(8;21)(q22;q22). Among CD19+ samples, we observed a continuum of CD19 expression levels on AML cells. In individuals exhibiting unimodal and high CD19 expression, the antigen was consistently present on nearly all CD34+CD38- and CD34+CD38+ subpopulations. In ex vivo AML-T cell co-cultures, blinatumomab demonstrated substantial AML killing, with an efficacy similar to BCP-ALL. In addition, CAR T cells could effectively eliminate CD19+ AML cells ex vivo. Furthermore, our immunogenomic assessment of the bone marrow immune microenvironment of newly diagnosed pediatric t(8;21) AML revealed that T- and NK cells had a less exhausted and senescent phenotype in comparison to pediatric BCP-ALL. Altogether, our study underscores the promise of CD19-directed immunotherapies for the treatment of pediatric CD19+ AML.

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