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Transcriptomic data of cord blood CD34+ cells as controls of transcriptome cohort of pediatric acute myeloid leukemia

ABSTRACT: Transcriptomic data of cord blood CD34+ cells as controls of transcriptome cohort of pediatric acute myeloid leukemia

PROVIDER: PRJNA786561 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17141919_1.fastq.gz	Fastqsanger.gz
	SRR17141919_2.fastq.gz	Fastqsanger.gz
	SRR17141920_1.fastq.gz	Fastqsanger.gz
	SRR17141920_2.fastq.gz	Fastqsanger.gz
	SRR17141921_1.fastq.gz	Fastqsanger.gz

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Transcriptomic data of cord blood CD34+ cells as controls of transcriptome cohort of pediatric acute myeloid leukemia

Project description:We established a transcriptome cohort of pediatric acute myeloid leukemia (n=553) with RNA sequencing. This dataset of cord blood CD34+ cells (n=5, indivisual lots) is normal controls to characterize leukemia-specific expression patterns.

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Project description:UBTF tandem duplications (UBTF-TD) were identified frequently in relapsed pediatric acute myeloid leukemia. The purpose of this study is to investigate the functional consequence of the overexpression of UBTF-TD in normal cord blood CD34+ cells.

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Transcription profiling of human AML1-ETO transduced cord blood cells, CD34 selected, compared to normal cord blood cells, CD34 selected

Project description:AML1-ETO expression in normal human umbilical cord blood CD34+ cells leads to long-term proliferation of an early self-renewing primitive progenitor cell with multilineage potential and stem cell ability, but these cells do not induce leukemia in immunodeficient mice. This comparative microarray study was initiated to determine the differences in the transcriptome of AML-ETO-expressing CD34+ cells after extended culture in vitro, using normal cord blood cells expanded for 6-8 weeks in vitro and subsequently purified for the CD34+ population as the control comparison. Experiment Overall Design: We have established a culture system whereby we retrovirally transduce human CD34+ cells, obtained from cord blood, with the leukemia fusion gene AML1-ETO. Cells expressing this fusion protein are able to proliferate long-term in vitro in a cytokine dependent manner. AML1-ETO-expressing cord blood cells have a large population of primitive self-renewing CD34+ cells with continued abnormal differentiation. We grow these cells in serum-free conditions using the BIT supplement from Stem Cell Technologies. For the current experiments we used cell cultures that had been proliferating in vitro for 8-12 weeks, in a cytokine cocktail of SCF, TPO, FLT3L, IL-6 all at 20 ng/mL and IL-3 at 10 ng/mL. Control cord blood samples that were CD34 purified were expanded for 5-8 weeks in the same culture media as used for AML1-ETO cells. All samples were magnetically selected for the CD34+ population, returned to culture, and one week later again selected for CD34+ cells and then lysed for RNA isolation.

2008-06-15 | E-GEOD-8023 | biostudies-arrayexpress

Epigenetic and molecular signatures of cord blood CD34(+) cells treated with histone deacetylase inhibitors

Project description:Gene expression profiling of primary cord blood hematopoietic stem cell (day 0, CD34+ cells), enriched control (untreated), Scriptaid and Valproic acid expanded CD34+ cells after a week in culture. Cord blood CD34+ cells were processed individually and equal number of PC and reisolated CD34+ cells from 3-4 samples were pooled after expansion to avoid sample variations.

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ADGRG1/GPR56 knockdown in cord blood CD34+ cells

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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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Project description:We have employed whole genome microarray expression profiling to identify genes differentially expressed in cord blood enriched CD34+ cells(>95%) after a short-term exposure to the chemokine stromal cell-derived factor-1 (SDF-1). SDF-1 induced gene expressions of cord blood enriched CD34+ cells were measured at 4 hours. Four biological replicates were performed for each treatment group.

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