Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cancer immunotherapy via synergistic co-activation of myeloid cells

ABSTRACT: Cancer immunotherapy via synergistic co-activation of myeloid cells

PROVIDER: PRJNA975167 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24652844.fastq.gz	Fastqsanger.gz
	SRR24652845.fastq.gz	Fastqsanger.gz
	SRR24652846.fastq.gz	Fastqsanger.gz
	SRR24652847.fastq.gz	Fastqsanger.gz
	SRR24652848.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 38

Similar Datasets

Cancer immunotherapy via synergistic co-activation of myeloid cells [RNA-seq]

Project description:Cancer immunotherapy via synergistic co-activation of myeloid cells [RNA-seq]

| PRJNA974099 | ENA

Cancer immunotherapy via synergistic co-activation of myeloid cells [scRNA-seq]

Project description:Cancer immunotherapy via synergistic co-activation of myeloid cells [scRNA-seq]

| PRJNA975171 | ENA

Cancer immunotherapy via synergistic co-activation of myeloid cells [RNA-seq]

Project description:Myeloid cells coordinate T cell immune evasion in cancer yet are pliable and possess anti-tumor potential. Here, by co-targeting activation molecules we leverage the myeloid compartment as a therapeutic vulnerability in cancer. Myeloid cells in solid tumors expressed activation receptors including the pattern recognition receptor CLEC7A and the TNF receptor superfamily member CD40. In mouse models of checkpoint inhibitor-resistant pancreatic cancer, co-activation of CLEC7A, via systemic β-glucan therapy, and CD40, with agonist antibody treatment, eradicated established tumors and induced immunological memory. Anti-tumor activity was dependent on a cDC1 – T cell axis but did not require classical T cell cytotoxicity or blockade of checkpoint molecules. Rather, targeting CD40 drove T cell-derived IFNγ signaling which converged with CLEC7A activation to program distinct macrophage subsets to facilitate tumor responses. Thus, productive cancer immune surveillance can be invoked by co-activation of complementary myeloid signaling pathways.

2023-11-10 | GSE232860 | GEO

Cancer immunotherapy via synergistic co-activation of myeloid cells

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

2023-11-10 | GSE233175 | GEO

Cancer immunotherapy via synergistic co-activation of myeloid cells [scRNA-seq]

Project description:The goal of this study was to define the impact of beta-glucan (CLEC7A agonist), anti-CD40 (agonist) and the combination of beta-glucan and anti-CD40 on the intra-tumoral immune landscape of mouse orthotopic pancreatic tumors using single-cell RNA sequencing.

2023-11-10 | GSE233171 | GEO

STING activation improves T-cell-engaging immunotherapy of acute myeloid leukemia

Project description:STING activation improves T-cell-engaging immunotherapy of acute myeloid leukemia

| PRJNA1065460 | ENA

Single-cell RNA sequencing reveals myeloid and T cell co-stimulation mediated by IL-7 anti-cancer immunotherapy

Project description:Single-cell RNA sequencing reveals myeloid and T cell co-stimulation mediated by IL-7 anti-cancer immunotherapy

| PRJNA844355 | ENA

Mapping the HLA ligandome landscape of acute myeloid leukemia: a targeted approach toward peptide-based immunotherapy

Project description:Identification of physiologically relevant peptide vaccine targets calls for the direct analysis of the entirety of naturally presented human leukocyte antigen (HLA) ligands, termed the HLA ligandome. In this study, we implemented this direct approach using immunoprecipitation and mass spectrometry to define acute myeloid leukemia (AML)-associated peptide vaccine targets. Mapping the HLA class I ligandomes of 15 AML patients and 35 healthy controls, more than 25 000 different naturally presented HLA ligands were identified. Target prioritization based on AML exclusivity and high presentation frequency in the AML cohort identified a panel of 132 LiTAAs (ligandome-derived tumor-associated antigens), and 341 corresponding HLA ligands (LiTAPs (ligandome-derived tumor-associated peptides)) represented subset independently in >20% of AML patients. Functional characterization of LiTAPs by interferon-γ ELISPOT (Enzyme-Linked ImmunoSpot) and intracellular cytokine staining confirmed AML-specific CD8+ T-cell recognition. Of note, our platform identified HLA ligands representing several established AML-associated antigens (e.g. NPM1, MAGED1, PRTN3, MPO, WT1), but found 80% of them to be also represented in healthy control samples. Mapping of HLA class II ligandomes provided additional CD4+ T-cell epitopes and potentially synergistic embedded HLA ligands, allowing for complementation of a multipeptide vaccine for the immunotherapy of AML.

2019-10-14 | PXD015748 | Pride

Genomewide Screen Reveals Potential Synergistic Partners for FLT3 Mutant Myeloid Leukemia

Project description:Genomewide Screen Reveals Potential Synergistic Partners for FLT3 Mutant Myeloid Leukemia

| PRJNA600003 | ENA

TREM2 blockade modifies the tumor myeloid landscape enhancing anti-PD-1 immunotherapy

Project description:Checkpoint immunotherapy unleashes T cell effector functions that control tumor growth, but can be undermined by myeloid cells that induce immunosuppression. TREM2 is a myeloid surface receptor that binds lipids and transmits intracellular signals through protein-tyrosine phosphorylation known to sustain microglial responses during Alzheimer’s disease. Intriguingly, TREM2 expression has recently been noted in tumor-infiltrating macrophages. We found that Trem2–/– mice are more resistant to growth of sarcoma, colorectal and mammary cancer cells than wild-type mice and are more responsive to anti-PD-1 immunotherapy. Furthermore, treatment with anti-TREM2 mAb curbed tumor growth and led to complete tumor regression when combined with anti-PD-1. scRNA-seq revealed that both constitutive TREM2 deficiency and anti-TREM2 are associated with relatively scant representation of MRC1+ and CX3CR1+ subsets in the macrophage tumor infiltrate, paralleled by expansion of subsets expressing immunostimulatory molecules. These changes were associated with improved T cell responses. TREM2 expression was evident in tumor macrophages in over 200 human cancer cases examined and inversely correlated with prolonged survival for two types of cancer. Thus, TREM2 is a promising target to modify tumor-infiltrating myeloid cells and effectively augment checkpoint immunotherapy.

2020-08-13 | GSE151710 | 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