Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell RNAseq analysis of wildtype and CaMKK2 KO immune infiltrate of CT2a preclinical murine glioma

ABSTRACT: Single-cell RNAseq analysis of wildtype and CaMKK2 KO immune infiltrate of CT2a preclinical murine glioma

PROVIDER: PRJNA812581 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Single-cell RNAseq analysis of wildtype and CaMKK2 KO immune infiltrate of CT2a preclinical murine glioma

Project description:CaMKK2 promotes a more pro-tumor and checkpoint blockade-resistance associated immune tumor microenvironment in glioblastoma.

2022-08-30 | GSE197879 | GEO

Effect of inhibition of LDHA using FX11 on gene expression in CT2A glioma cells

Project description:To investigate the role of LDHA in regulating gene expression in glioma cells, we treated CT2A glioma cells with LDHA inhibitor FX11. We then performed gene expression profiling analysis using data obtained from RNA-seq of control and FX11-treated cells.

2023-11-09 | GSE216070 | GEO

Antigen presentation deficiency, mesenchymal differentiation, and resistance to immunotherapy in the murine syngeneic CT2A tumor model

Project description:A common cornerstone of preclinical cancer research is the use of syngeneic orthotopic murine tumors as immunocompetent models of human cancers. For glioblastoma research efforts, the GL261 and CT2A lines are frequently used. We systematically characterized these two lines to decipher the cell-intrinsic mechanisms that drive immuno-resistance in CT2A and to define the aspects of human cancer biology that the lines best model. We show that, despite sharing a few canonical genetic or histologic features of human glioblastoma, the transcriptional profiles of GL261 and CT2A tumours most closely resembled those of glioblastomas. CT2A additionally resembled other cancer types transcriptionally, including melanoma. CT2A displayed mesenchymal differentiation, upregulated angiogenesis, and multiple defects in antigen presentation machinery and interferon response pathways. Loss of MHC class I expression was restored in CT2A by interferon-γ treatment, explaining in part the modest efficacy of some immunotherapy combinations for CT2A. Our findings indicate that CT2A may serve as a robust preclinical solid tumor model of adaptive immune resistance.

2023-12-19 | PXD036720 | Pride

Effects of the treatment with IFNβ and GM-CSF-secreting CT2A cells to wildtype CT2A tumor microenvironment post resection

Project description:To elucidate the underlying immune responses elicited by IFNβ and GM-CSF-secreting CT2A cells to brain tumor microenvironment post resection compared to placebo group and non-IFNβ and GM-CSF-secreting CT2A cell group

2022-11-09 | GSE217253 | GEO

Transcriptional analysis of ATRX deficiency in a CT2A glioma model

Project description:Transcriptional analysis of ATRX deficiency in a CT2A glioma model

| PRJNA949116 | ENA

Effect of inhibition of LDHA using FX11 on gene expression in CT2A glioma cells

Project description:Effect of inhibition of LDHA using FX11 on gene expression in CT2A glioma cells

| PRJNA892026 | ENA

RNAseq of tumor endothelial cells isolated from CT2A glioma under control or LGK974 treatment

Project description:RNAseq of tumor endothelial cells isolated from CT2A glioma under control or LGK974 treatment

| PRJNA839710 | ENA

Transcriptional analysis of co-occuring ATRX deficiency and IDH1 mutation in a CT2A glioma model

Project description:Transcriptional analysis of co-occuring ATRX deficiency and IDH1 mutation in a CT2A glioma model

| PRJNA948443 | ENA

Effects of the treatment with IFNβ and GM-CSF-secreting CT2A cells to wildtype CT2A tumor microenvironment post resection

Project description:Effects of the treatment with IFNβ and GM-CSF-secreting CT2A cells to wildtype CT2A tumor microenvironment post resection

| PRJNA898299 | ENA

Transcriptional analysis of ATRX deficiency in a CT2A glioma model

Project description:Stimulating the innate immune system has been explored as a therapeutic option for the treatment of gliomas. Inactivating mutations in ATRX, a defining molecular alteration in IDH-mutant astrocytomas, have been implicated in dysfunctional immune signaling. However, little is known about the interplay between ATRX loss and IDH mutation on innate immunity. To explore this biology, we generated ATRX knockout glioma models in the presence and absence of the IDH1R132H mutation. ATRX-deficient glioma cells were sensitive to dsRNA-based innate immune agonism and exhibited impaired lethality and increased T-cell infiltration in vivo. However, the presence of IDH1R132H dampened baseline expression of key innate immune genes and cytokines in a manner restored by genetic and pharmacological IDH1R132H inhibition. IDH1R132H co-expression did not interfere with the ATRX KO-mediated sensitivity to dsRNA. Thus, ATRX loss primes cells for recognition of dsRNA, while IDH1R132H reversibly masks this priming. This work reveals innate immunity as a therapeutic vulnerability of astrocytoma.

2023-03-31 | GSE228242 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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