Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML[RNA]

ABSTRACT: We identified BATF as a core transcription factor and the main mediator of this NK cell dysfunction in AML. our findings reveal a previously unidentified mechanism of NK immune evasion in AML manifested by epigenetic rewiring and inactivation of NK cells by myeloid blasts.  This work highlights the importance of using healthy allogeneic NK cells as adoptive cell therapy to treat patients with myeloid malignancies combined with strategies aimed at preventing the dysfunction by targeting the TGF-b pathway or BATF

ORGANISM(S): Homo sapiens

PROVIDER: GSE273750 | GEO | 2024/08/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML[ATAC-seq]

Project description:We identified BATF as a core transcription factor and the main mediator of this NK cell dysfunction in AML. our findings reveal a previously unidentified mechanism of NK immune evasion in AML manifested by epigenetic rewiring and inactivation of NK cells by myeloid blasts.  This work highlights the importance of using healthy allogeneic NK cells as adoptive cell therapy to treat patients with myeloid malignancies combined with strategies aimed at preventing the dysfunction by targeting the TGF-b pathway or BATF

2024-08-31 | GSE273747 | GEO

BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML[CUT&RUN]

2024-08-31 | GSE273749 | GEO

BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML[RNA]

Project description:BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML[RNA]

| PRJNA1143026 | ENA

BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML[ATAC-seq]

Project description:BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML[ATAC-seq]

| PRJNA1142983 | ENA

BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML[CUT&RUN]

Project description:BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML[CUT&RUN]

| PRJNA1143027 | ENA

Defective NK cells in AML patients at diagnosis are associated with blast transcriptional signatures of immune evasion

Project description:Acute myeloid leukemia (AML) is a heterogeneous group of malignancies which may be sensitive to the natural killer (NK) cell anti-tumor response. However, NK cells are frequently defective in AML. Here, we found in an exploratory cohort (n = 46) that NK-cell status at diagnosis of AML separated patients in two groups with a different clinical outcome. Patients with a deficient NK-cell profile, including reduced expression of some activating NK receptors (e.g. DNAM-1, NKp46 and NKG2D) and decreased IFN-g production, had a significantly higher risk of relapse (P = 0.03) independently of cytogenetic classification in multivariate analysis. Patients with defective NK cells showed a profound gene expression decrease in AML blasts for cytokine and chemokine signaling (e.g. IL15, IFNGR1, IFNGR2, CXCR4), antigen processing (e.g. HLA-DRA, HLA-DRB1, CD74) and adhesion molecule pathways (e.g. PVR, ICAM1). A set of 388 leukemic classifier genes defined in the exploratory cohort was independently validated in a multicentric cohort of 194 AML patients. In total, these data evidenced the interplay between NK-cells and AML blasts at diagnosis allowing an immune-based stratification of AML patients independently of clinical classifications. 5 normal AML cells were compared with 8 NK deficient AML cells.

2015-07-24 | E-GEOD-50928 | biostudies-arrayexpress

Defective NK cells in AML patients at diagnosis are associated with blast transcriptional signatures of immune evasion

Project description:Acute myeloid leukemia (AML) is a heterogeneous group of malignancies which may be sensitive to the natural killer (NK) cell anti-tumor response. However, NK cells are frequently defective in AML. Here, we found in an exploratory cohort (n = 46) that NK-cell status at diagnosis of AML separated patients in two groups with a different clinical outcome. Patients with a deficient NK-cell profile, including reduced expression of some activating NK receptors (e.g. DNAM-1, NKp46 and NKG2D) and decreased IFN-g production, had a significantly higher risk of relapse (P = 0.03) independently of cytogenetic classification in multivariate analysis. Patients with defective NK cells showed a profound gene expression decrease in AML blasts for cytokine and chemokine signaling (e.g. IL15, IFNGR1, IFNGR2, CXCR4), antigen processing (e.g. HLA-DRA, HLA-DRB1, CD74) and adhesion molecule pathways (e.g. PVR, ICAM1). A set of 388 leukemic classifier genes defined in the exploratory cohort was independently validated in a multicentric cohort of 194 AML patients. In total, these data evidenced the interplay between NK-cells and AML blasts at diagnosis allowing an immune-based stratification of AML patients independently of clinical classifications. Gene expression analysis were performed on CD56bright and CD56dim NK cells sorted from patients with impaired or normal CD56bright NK cells (n=2 for each patients? group) and from 3 HC

2015-07-24 | E-GEOD-34885 | biostudies-arrayexpress

CITE-seq of CAR-NK cells

Project description:Primary chimeric antigen receptor (CAR) natural killer (NK) cells show strong cytotoxic efficacy against acute myeloid leukemia (AML) in vivo. However, NK cell-mediated tumor killing is often impaired by tumor-mediated immune cell inactivation. Here, we report a novel strategy to overcome NK cell inhibition caused by the immune checkpoint NKG2A, which interacts with HLA-E expressed on AML blasts. We generated AML-specific CD33-directed CAR (CAR33)-KLRC1ko-NK cells with CRISPR/Cas9-based gene editing of the NKG2A-encoding KLRC1 gene. Single-cell multi-omic analyses revealed a higher proportion of activated cells in CAR33-NK- and CAR33-KLRC1ko-NK pools, which were preserved following AML-cell contact. This activated state of the CAR33-KLRC1ko-NK cells has been translated into improved antileukemic activity in vitro and in vivo against AML cell lines and primary blasts. This dual modification of primary NK cells has the potential to bypass the suppressive effect not only of AML but also in a broad range of other cancer identities.

2024-07-16 | GSE221552 | GEO

Defective NK cells in AML patients at diagnosis are associated with blast transcriptional signatures of immune evasion

2015-07-24 | GSE50928 | GEO

Defective NK cells in AML patients at diagnosis are associated with blast transcriptional signatures of immune evasion

2015-07-24 | GSE34885 | GEO