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CD19 CAR immune pressure on B cell acute lymphoblastic leukemia induces myeloid lineage switch exposing inherent leukemic plasticity

ABSTRACT: CD19 CAR immune pressure on B cell acute lymphoblastic leukemia induces myeloid lineage switch exposing inherent leukemic plasticity

PROVIDER: PRJNA325272 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3656550.fastq.gz	Fastqsanger.gz
	SRR3656560_1.fastq.gz	Fastqsanger.gz
	SRR3656560_2.fastq.gz	Fastqsanger.gz
	SRR3656551.fastq.gz	Fastqsanger.gz
	SRR3656561_1.fastq.gz	Fastqsanger.gz

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CD19 CAR immune pressure on B cell acute lymphoblastic leukemia induces myeloid lineage switch exposing inherent leukemic plasticity (RNA-Seq)

Project description:This study establishs lineage switch as a mechanism of CAR resistance exposing inherent plasticity in genetic subtypes of pre-B cell ALL

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CD19 CAR immune pressure on B cell acute lymphoblastic leukemia induces myeloid lineage switch exposing inherent leukemic plasticity (ChIP-Seq)

Project description:This study establishs lineage switch as a mechanism of CAR resistance exposing inherent plasticity in genetic subtypes of pre-B cell ALL

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CD19 CAR immune pressure on B cell acute lymphoblastic leukemia induces myeloid lineage switch exposing inherent leukemic plasticity

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-02-10 | GSE83205 | GEO

CD19 CAR immune pressure induces B-precursor acute lymphoblastic leukaemia lineage switch exposing inherent leukaemic plasticity.

Project description:Adoptive immunotherapy using chimeric antigen receptor (CAR) expressing T cells targeting the CD19 B lineage receptor has demonstrated marked success in relapsed pre-B-cell acute lymphoblastic leukaemia (ALL). Persisting CAR-T cells generate sustained pressure against CD19 that may drive unique mechanisms of resistance. Pre-B ALL originates from a committed pre-B cell or an earlier progenitor, with potential to reprogram into other hematopoietic lineages. Here we report changes in lineage markers including myeloid conversion in patients following CD19 CAR therapy. Using murine ALL models we study the long-term effects of CD19 CAR-T cells and demonstrate partial or complete lineage switch as a consistent mechanism of CAR resistance depending on the underlying genetic oncogenic driver. Deletion of Pax5 or Ebf1 recapitulates lineage reprogramming occurring during CD19 CAR pressure. Our findings establish lineage switch as a mechanism of CAR resistance exposing inherent plasticity in genetic subtypes of pre-B-cell ALL.

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Single-cell profiling identifies pre-existing CD19-negative subclones in a B-ALL patient with CD19-negative relapse after CAR-T therapy

Project description:Chimeric antigen receptor T cell (CAR-T) targeting the CD19 antigen represents an innovative therapeutic approach to improve the outcome of relapsed or refractory B-cell acute lymphoblastic leukemia (B-ALL). Yet, despite a high initial remission rate, CAR-T therapy ultimately fails for some patients. Notably, around half of relapsing patients develop CD19 negative (CD19neg) B-ALL allowing leukemic cells to evade CD19-targeted therapy. Herein, we investigate leukemic cells of a relapsing B-ALL patient, at two-time points: before (T1) and after (T2) anti-CD19 CAR-T treatment. We show that at T2, the B-ALL relapse is CD19 negative due to the expression of a non-functional CD19 transcript retaining intron 2. Then, using single-cell RNA sequencing (scRNAseq) approach, we demonstrate that CD19neg leukemic cells were present before CAR-T cell therapy and thus that the relapse results from the selection of these rare CD19neg B-ALL clones. In conclusion, our study shows that scRNAseq profiling can reveal pre-existing CD19neg subclones, raising the possibility to assess the risk of targeted therapy failure.

2020-12-11 | GSE153697 | GEO

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Project description:CD19 CAR immune pressure on B cell acute lymphoblastic leukemia induces myeloid lineage switch exposing inherent leukemic plasticity (RNA-Seq)

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Project description:CD19 CAR immune pressure on B cell acute lymphoblastic leukemia induces myeloid lineage switch exposing inherent leukemic plasticity (ChIP-Seq)

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Proteomic changes of CD19+ B Lymphocytes in COVID-19 Patients

Project description:The immune response to SARS-CoV-2 varies among patients. We used proteomic analysis to study CD19+ lymphocytes, which are important for the immune response. By comparing the proteomes of CD19+ cells from healthy individuals and COVID-19 patients, we discovered proteins and signaling pathways involved in the immune response during COVID-19. This knowledge improves our understanding of immune dysregulation in COVID-19 and can help develop targeted therapies. Our research also explores the role of CD19+ lymphocytes in COVID-19 and identifies potential biomarkers. Overall, our findings contribute to understanding COVID-19 immunology and inform future research efforts.

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2024-08-08 | GSE270185 | GEO

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Project description:Leukemic hematopoiesis

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