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RNA sequencing of CD19-directed chimeric antigen receptor T (CART19) cells with and without TP-0903 treatment

ABSTRACT: RNA sequencing of CD19-directed chimeric antigen receptor T (CART19) cells with and without TP-0903 treatment

PROVIDER: PRJNA819068 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18455300_1.fastq.gz	Fastqsanger.gz
	SRR18455300_2.fastq.gz	Fastqsanger.gz
	SRR18455301_1.fastq.gz	Fastqsanger.gz
	SRR18455301_2.fastq.gz	Fastqsanger.gz
	SRR18455302_1.fastq.gz	Fastqsanger.gz

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RNA sequencing of CD19-directed chimeric antigen receptor T (CART19) cells with and without TP-0903 treatment

Project description:TP-0903 was obtained from Tolero Pharmaceuticals. CART19 cells from five biological replicates were thawed and stimulated with irradiated Jeko-1 cells (120 Gy) for 5 days. Jeko-1 is a human mantle cell lymphoma cell line that expresses the CD19 antigen (ATCC). Each sample was treated with either 30 nM TP0903 (treated condition) or DMSO (untreated control). CART19 were isolated to a purity of 100% using CD19 microbeads (Miltenyi). RNA was isolated from the CART19 using QIAGEN RNeasy Plus Mini Kit (Cat. No. 74134). RNA was further treated with DNase I and purified using Zymo Research RNA Clean & Concentrator (Cat. No. R1015).

2023-10-04 | GSE199257 | GEO

Epigenetic profiling and response to CD19 chimeric antigen receptor (CAR) T-cell therapy in B-cell malignancies

Project description:Chimeric antigen receptor (CAR) T-cells directed against CD19 (CART19) are effective in relapsed/refractory (R/R) B-cell malignancies. Not all patients show treatment efficacy, but little is known about the molecular factors predicting clinical outcome of CART19 therapy. Our objective was to determine the effect of epigenetic changes in CART19 cells on the clinical course of B-cell malignancy patients treated with adoptive therapy. We report a case series of B-cell malignancy patients (68 males (M) and 46 females (F); median age of 24 years (range 3-70 years)), comprising 77 acute lymphoblastic leukemia (ALL) cases and 37 non-Hodgkin lymphoma (NHL) cases, who were treated with CART19 cells. Using a DNA methylation microarray, we determined the epigenomic changes that occur in the patient T-cells upon transduction of the CAR vector. We identified 984 genomic sites with differential DNA methylation between CAR-untransduced (UT) and CAR-transduced (TD) T-cells before infusion into the patient. 18 of these distinct epigenetic loci were significantly associated with complete response (CR). Using the sites linked to CR, the EPICART signature was established, which was associated with enhanced overall survival (OS).

2021-08-23 | GSE179414 | GEO

Transcriptional profiling of CART19 cells exposed to WT and BIDko Nalm6 cells

Project description:Cellular immunotherapy using T cells engineered to express chimeric antigen receptors targeting CD19 (CART19) leads to long-term remission in patients with B-cell malignancies1-5. Unfortunately, a significant fraction of patients demonstrate primary resistance to CART19 or experience relapse after achieving remission. Beyond loss of target antigen, the molecular pathways governing CART19 failure are unknown. Here we demonstrate that death receptors, cell surface signaling molecules that induce target cell apoptosis, are key mediators of leukemic resistance and CART19 failure. Using a functional CRISPR/Cas9-based genome-wide knockout screen6 in B-cell acute lymphoblastic leukemia (ALL), we identified the death receptor signaling pathway as a central regulator of sensitivity to CART19-induced cell death. In the absence of the pro-apoptotic death receptor signaling molecules BID or FADD, ALL cells were resistant to CART19 cytotoxicity, resulting in rapid disease progression in mice. We found that this initial resistance to cytotoxicity led to persistence of tumor cells, which drove the development of T cell dysfunction that further compromised anti-tumor immunity and permitted tumor outgrowth. We validated these findings using clinical samples collected from patients with ALL treated with CD19-targeted CAR T cells and found that expression of pro-apoptotic death receptor pathway genes in pre-treatment tumor samples correlated with CAR T cell expansion and persistence, as well as patient response and overall survival. Our findings indicate that tumor-intrinsic death receptor signaling directly contributes to CAR T cell failure.

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ATAC profiling of CART19 cells exposed to WT and BIDko Nalm6 cells

2020-02-17 | GSE130818 | GEO

Genome-wide CRISPR/Cas9 guide library knockout screening in Nalm6 ALL cells under CART19 selective pressure

2020-02-17 | GSE130819 | GEO

mRNA profiling on CD19-directed chimeric antigen receptor T (CART19) cells with and without platelet-poor plasma from untreated chronic lymphocytic leukemia (CLL) patients (CLL-derived extracellular vesicles)

Project description:mRNA profiling on CD19-directed chimeric antigen receptor T (CART19) cells with and without platelet-poor plasma from untreated chronic lymphocytic leukemia (CLL) patients (CLL-derived extracellular vesicles)

| PRJNA612847 | ENA

mRNA profiling on GM-CSF knockout CART19 compared to wildtype CART19 and Ctrl gRNA CART19 produced from normal donors

Project description:RNA sequencing was performed on three biological replicates of CART19 (GM-CSF wildtype), GM-CSF knockout CART19, and Ctrl gRNA CART19 produced from normal donors.

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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.

2024-08-08 | GSE270185 | GEO

mRNA profiling on Axl inhibitor TP0903 treated CART19 compared to untreated CART19 produced from normal donors

Project description:RNA sequencing was performed on three biological replicates of DMSO treated CART19 (control) and TP0903 treated CART19 produced from normal donors.

2023-08-31 | GSE231611 | GEO

Expression data from mouse CD19-targeted CAR (chimeric antigen receptor) T cells after antigen stimulation [expression array]

Project description:Second-generation CD19-targeted chimeric antigen receptors (CAR) have an antigen-binding domain fused to transmembrane, co-stimulatory, and CD3ζ domains. The two CARs with regulatory approval include a CD28 or 4-1BB co-stimulatory domain. While both CARs achieve similar clinical outcomes, biologic differences between the two endodomains have become apparent but not completely understood. The objective is to evaluate gene expression in different mouse CD19-targeted CAR T cells, including m19z, m1928z and m19-musBBz.

2018-07-31 | GSE111641 | GEO

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