Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nr4a transcription factors limit CAR-T cell function in solid tumors [RNA-Seq]

ABSTRACT: Chromatin accessibility with ATAC-seq and gene expression with RNA-seq for CD8 T cells expressing chimeric antigen receptors in solid tumors or after in vitro culture.

ORGANISM(S): Mus musculus

PROVIDER: GSE123738 | GEO | 2019/02/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Nr4a transcription factors limit CAR-T cell function in solid tumors [ATAC-Seq]

Project description:Chromatin accessibility with ATAC-seq and gene expression with RNA-seq for CD8 T cells expressing chimeric antigen receptors in solid tumors or after in vitro culture.

2019-02-13 | GSE123629 | GEO

Nr4a transcription factors limit CAR-T cell function in solid tumors [ATAC-Seq]

Project description:Nr4a transcription factors limit CAR-T cell function in solid tumors [ATAC-Seq]

| PRJNA509426 | ENA

Nr4a transcription factors limit CAR-T cell function in solid tumors

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

2019-02-13 | GSE123739 | GEO

Nr4a transcription factors limit CAR-T cell function in solid tumors

Project description:Nr4a transcription factors limit CAR-T cell function in solid tumors

| PRJNA509664 | ENA

NR4A transcription factors limit CAR T cell function in solid tumours.

Project description: Not available

| S-EPMC6546093 | biostudies-literature

Nr4a transcription factors limit CAR-T cell function in solid tumors [RNA-Seq]

Project description:Nr4a transcription factors limit CAR-T cell function in solid tumors [RNA-Seq]

| PRJNA509668 | ENA

The Second Generation of CAR-iMACs with Enhanced Polarization, CAR-mediated Efferocytosis and Superior Potency against Solid Tumors

Project description:Chimeric antigen receptor (CAR)-T cell therapies have shown great success in treating hematologic malignancies. Nonetheless, their therapeutic effect on solid tumors remains to be improved. Recently, macrophages have attracted great attention, given their ability to infiltrate solid tumors, phagocytize tumor cells as well as their immunomodulatory capacities. The first generation of CD3ζ-based CAR-macrophages demonstrated that the CAR could stimulate macrophage phagocytosis in a tumor antigen-dependent way. Here, we genetically engineered induced pluripotent stem cell (iPSC)-derived macrophages (iMACs) with TLR4 intracellular TIR domain-containing CARs against EGFRvIII and GPC3, which yielded markedly enhanced antitumor effect in two different solid tumor models including glioblastoma, and hepatocellular carcinoma in which complete remission was achieved with CAR-iMACs alone or in combination with CD47 antibody. Moreover, the tandem CD3ζ-TIR-CAR, or the “second-generation” design of TIR-based dual signaling CAR, endowed iMACs with both target engulfment/efferocytosis capacity against antigen-expressing solid tumor cells, and potency of antigen-dependent M1 state polarization and M2 state resistance in an NF-κB dependent manner. We also illustrated a surprising mechanism of tumor cell elimination by CAR-induced efferocytosis against tumor cell apoptotic bodies. Taken together, we established the next generation CAR-iMACs equipped with orthogonal phagocytosis and polarization capacity for better antitumor functions in treating solid tumors.

2023-09-29 | GSE214140 | GEO

c-Kit signaling potentiates CAR T-cell efficacy in solid tumors by CD28- and IL-2–independent costimulation

Project description:The limited efficacy of chimeric antigen receptor (CAR) T-cell therapy for solid tumors necessitates engineering strategies that promote functional persistence in an immunosuppressive environment. Herein, we exploit c-Kit signaling, a physiological pathway associated with stemness in hematopoietic progenitor cells (T cells lose expression of c-Kit during differentiation). CAR T cells with intracellular expression—but no cell-surface receptor expression—of the c-Kit D816V mutation (KITv) have upregulated STAT phosphorylation, antigen-activation-dependent proliferation, CD28- and IL-2–independent and IFN-γ–mediated costimulation, augmenting the cytotoxicity of first-generation CAR T cells. This translates to enhanced survival, including in TGF-β–rich and low-antigen-expressing solid tumor models. KITv CAR T cells have equivalent or better in vivo efficacy than second-generation CAR T cells and are susceptible to tyrosine kinase inhibitors (safety switch). When combined with CD28 costimulation, KITv costimulation functions as a third signal, enhancing efficacy and providing a potent approach to treat solid tumors.

2023-04-24 | GSE229026 | GEO

Epigenetically programmed ‘stem-like’ tissue resident memory CAR T-cells exhibit robust activity against solid and liquid tumors [scRNA]

Project description:Chimeric antigen receptor (CAR) T-cells have shown remarkable success in the therapy of hematological malignancies, but they have not yet proven nearly as effective in treating non-hematopoietic cancers. This study proposes augmentation of CAR T-cell function and accumulation in solid tumors by modifying the epigenetic landscape that governs early memory differentiation and adaptation to tissue residency. We identified that a key factor in human tissue-resident memory CAR T-cell (CAR-TRM) formation is activation in the presence of the pleotropic cytokine, TGF-β, which epigenetically enforces a core transcriptional program of both ‘stemness’ and sustained tissue residency. This strategy results in a readily actionable in vitro production method for engineering peripheral blood T-cells into large numbers of ‘stem-like’ CAR-TRM cells resistant to epigenetically-imposed exhaustion that possess enhanced ability to accumulate in situ and rapidly kill cancer cells for more effective immunotherapy.

2023-02-23 | GSE224865 | GEO

Epigenetically programmed ‘stem-like’ tissue resident memory CAR T-cells exhibit robust activity against solid and liquid tumors [bulk_RNA]

2023-02-23 | GSE224864 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data