Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single cell transcriptomics of the tumor immune microenvironment from checkpoint blockade-treated KPC tumors

ABSTRACT: Single cell transcriptomics of the tumor immune microenvironment from checkpoint blockade-treated KPC tumors

PROVIDER: PRJNA851755 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19782500.fastq.gz	Fastqsanger.gz
	SRR19782501.fastq.gz	Fastqsanger.gz
	SRR19782502.fastq.gz	Fastqsanger.gz
	SRR19782503.fastq.gz	Fastqsanger.gz
	SRR19782504.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Single cell transcriptomics of the tumor immune microenvironment from checkpoint blockade-treated KPC tumors

Project description:Single cell transcriptomes of CD45+ cells from KPC tumor subcutaneous allografts, either treated with PD-1+CTLA-4 checkpoint blockade or treatment-naïve.

2022-08-01 | GSE206668 | GEO

Landscape of immune checkpoint blockade-induced immune alterations in the microenvironment of primary and metastatic brain tumors

Project description:Brain tumors reside in an immune privileged microenvironment where inflammatory processes are heavily regulated. Nevertheless, our recent study showed a significant immune infiltration in recurrent glioblastoma (rGBM) treated with neoadjuvant PD-1 checkpoint blockade therapy. Compared to GBM, the intracranial immunotherapy response of brain metastases (BrM) has been much less studied. Therefore we studied the effect of pre-surgical immune checkpoint blockade (ICB) on the immune compartments of BrM, using multiplex immunofluorescence, mass cytometry and single-cell RNA sequencing. ICB induced much higher T cell infiltration in BrM compared to rGBM. It also caused the loss of a unique perivascular macrophage subset (CD206+LYVE1+), the absence of which associated with the enhanced T cell infiltration in BrM. These T cells produced high levels of IFN-γ that elicited and interferon response transcriptional program in the tumor-associated myeloid cells. T cell-myeloid interactions were also strengthened by ICB in BrM and might have led to the terminal exhaustion of the infiltrating T cells. Our results emphasize the importance of adopting novel immune-boosting approaches to rejuvenate the systemic T cell pool so as to improve tumor control of brain metastases.

2023-07-06 | GSE193745 | GEO

Tumour mtDNA mutations drive aerobic glycolysis to enhance checkpoint blockade

Project description:Mitochondrial DNA (mtDNA) encodes essential machinery for respiration and metabolic homeostasis but is paradoxically among the most common targets of somatic mutations in the cancer genome, with truncating mutations in complex I genes being over-represented1 . While mtDNA mutations have been associated with both improved and worsened prognoses in several cancer lineages1–3, whether these mutations are drivers, or exert any functional effect on tumour biology remains controversial. Here we discover that complex I-encoding mtDNA mutations are sufficient to remodel the tumour immune landscape and therapeutic resistance to immune checkpoint blockade. Using mtDNA base editing technology we engineered recurrent truncating mutations in the mtDNA-encoded complex I gene, Mt-Nd5, into murine models of melanoma. Mechanistically, these mutations promoted utilisation of pyruvate as a terminal electron acceptor and increased glycolytic flux driven by an over-reduced NAD pool and NADH shuttling between GAPDH and MDH1, mediating a Warburg-like metabolic shift. In turn, without modifying tumour growth, this altered cancer cell-intrinsic metabolism reshaped the tumour microenvironment of mouse and human cancer in a mutation load-dependent fashion, encouraging an anti-tumour immune response. This subsequently sensitises both mouse and human cancers with high mtDNA mutant heteroplasmy to immune checkpoint blockade. Strikingly, patient lesions bearing >50% mtDNA mutation load demonstrated a >2.5-fold improved response rate to checkpoint inhibitor blockade. Taken together these data nominate mtDNA mutations as functional regulators of cancer metabolism and tumour biology, with potential for therapeutic exploitation and treatment stratification.

2023-11-08 | PXD039705 | Pride

Tumour mtDNA mutations drive aerobic glycolysis to enhance checkpoint blockade (part 2)

2023-11-08 | PXD044987 | Pride

Concurrent delivery of immune checkpoint blockade improves tumor microenvironment for vaccine-generated immunity

Project description:Concurrent delivery of immune checkpoint blockade improves tumor microenvironment for vaccine-generated immunity

| PRJNA741385 | ENA

Antibody-lectin chimeras for glyco-immune checkpoint blockade

Project description:Despite the curative potential of checkpoint blockade immunotherapy, most patients remain unresponsive to existing treatments. Glyco-immune checkpoints – interactions of cell-surface glycans with lectin, or glycan-binding, immunoreceptors – have emerged as prominent mechanisms of immune evasion and therapeutic resistance in cancer. Here, we describe antibody-lectin chimeras (AbLecs), a modular platform for glyco-immune checkpoint blockade. AbLecs are bispecific antibody-like molecules comprising a cell-targeting antibody domain and a lectin “decoy receptor” domain that directly binds glycans and blocks their ability to engage inhibitory lectin receptors. AbLecs potentiate anticancer immune responses including phagocytosis and cytotoxicity, outperforming most existing therapies and combinations tested. By targeting a distinct axis of immunological regulation, AbLecs synergize with blockade of established immune checkpoints. AbLecs can be readily designed to target numerous tumor and immune cell subsets as well as glyco-immune checkpoints, and therefore represent a new modality for cancer immunotherapy.

2025-08-13 | PXD063934 | Pride

Targeting Glycomes Sensitizes Ovarian Tumors to Immune Checkpoint Blockade

Project description:Targeting Glycomes Sensitizes Ovarian Tumors to Immune Checkpoint Blockade

| PRJNA1020891 | ENA

Single cell transcriptomics of the tumor immune microenvironment from checkpoint blockade-treated and/or TBK1 inhibitor-treated B16-OVA tumors

Project description:Single cell transcriptomics of the tumor immune microenvironment from checkpoint blockade-treated and/or TBK1 inhibitor-treated B16-OVA tumors

| PRJNA897814 | ENA

Landscape of immune checkpoint blockade-induced immune alterations in the microenvironment of primary and metastatic brain tumors

Project description:Landscape of immune checkpoint blockade-induced immune alterations in the microenvironment of primary and metastatic brain tumors

| PRJNA797449 | ENA

Tumour mitochondrial DNA mutations drive aerobic glycolysis to enhance checkpoint blockade

Project description:The mitochondrial genome encodes essential machinery for respiration and metabolic homeostasis but is paradoxically among the most common targets of somatic mutation in the cancer genome, with truncating mutations in respiratory complex I genes being most over-represented1. While mitochondrial DNA (mtDNA) mutations have been associated with both improved and worsened prognoses in several tumour lineages, whether these mutations are drivers or exert any functional effect on tumour biology remains controversial. Here we discovered that complex I-encoding mtDNA mutations are sufficient to remodel the tumour immune landscape and therapeutic resistance to immune checkpoint blockade. Using mtDNA base editing technology we engineered recurrent truncating mutations in the mtDNA-encoded complex I gene, Mt-Nd5, into murine models of melanoma. Mechanistically, these mutations promoted utilisation of pyruvate as a terminal electron acceptor and increased glycolytic flux driven by an over-reduced NAD pool and NADH shuttling between GAPDH and MDH1, mediating a Warburg-like metabolic shift. In turn, without modifying tumour growth, this altered cancer cell-intrinsic metabolism reshaped the tumour microenvironment promoting an anti-tumour immune response characterised by loss of resident neutrophils. This subsequently sensitised tumours bearing high mtDNA mutant heteroplasmy to immune checkpoint blockade, with phenocopy of key metabolic changes being sufficient to mediate this effect. Strikingly, patient lesions bearing >50% mtDNA mutation heteroplasmy also demonstrated a >2.5-fold improved response rate to checkpoint inhibitor blockade. Taken together these data nominate mtDNA mutations as functional regulators of cancer metabolism and tumour biology, with potential for therapeutic exploitation and treatment stratification.

2023-03-13 | MSV000091475 | MassIVE

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