Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The Immune Landscape of Tumor-Associated Macrophage Reprogramming.

ABSTRACT: The Immune Landscape of Tumor-Associated Macrophage Reprogramming.

PROVIDER: PRJNA1146352 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30186214.fastq.gz	Fastqsanger.gz
	SRR30186215.fastq.gz	Fastqsanger.gz
	SRR30186216.fastq.gz	Fastqsanger.gz
	SRR30186217.fastq.gz	Fastqsanger.gz
	SRR30186218.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

The Immune Landscape of Tumor-Associated Macrophage Reprogramming.

Project description:Tumor-associated macrophages (TAMs) generally acquire an immunosuppressive and tumor-promoting phenotype, which may contribute to tumor resistance to immunotherapy. We previously showed that suppression of microRNA activity through genetic Dicer1 inactivation rewires TAM’s transcriptomes and prompts their immunostimulatory activation. This phenotypic switch enhanced recruitment and activation of CD8+ cytotoxic T cells (CTLs) and improved the efficacy of immunotherapy in mouse cancer models. Here, we performed single-cell RNA sequencing of whole tumors grown in either wild-type mice or mice with macrophage-specific Dicer1 deletion. The analysis of multiple cell populations, including several discrete monocyte and macrophage subsets, indicated broad and convergent immunostimulatory programming of the tumor microenvironment (TME), which was dependent on CTL-derived interferon-gamma (IFNγ), in mice with DICER-deficient macrophages. Intriguingly, dynamic inferences on monocyte/macrophage ontogeny and differentiation by pseudotime analysis revealed trajectories associated with progression into cell cycle, monocyte-to-macrophage differentiation, and transition from an immunostimulatory to an immunosuppressive phenotype in tumors with DICER-proficient macrophages. Dicer1 deficiency interfered with this trajectory and stalled TAMs at an intermediate state between immature monocytes and macrophages with T cell-stimulatory capacity, thereby impeding immunosuppressive TAM development. This translated into enhanced response to antiangiogenic immunotherapy in an immunotherapy-resistant model of non-small cell lung cancer. Cycling/M2-like macrophages were conserved in human melanoma and hepatocellular carcinoma and should represent a more promising therapeutic target than the bulk of TAMs.

2025-03-31 | GSE274402 | GEO

Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis

Project description:Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis

| PRJNA1005936 | ENA

Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis [RNA-seq]

Project description:Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis [RNA-seq]

| PRJNA1104231 | ENA

Impact of HSC-derived immune training on granulocyte/macrophage progenitor chromatin landscape

Project description:Impact of HSC-derived immune training on granulocyte/macrophage progenitor chromatin landscape

| PRJNA845805 | ENA

WDR4 Drives Tumor-Associated Macrophage Reprogramming and Tumor Progression via eIF4E-Mediated mRNA Translation

Project description:WDR4 Drives Tumor-Associated Macrophage Reprogramming and Tumor Progression via eIF4E-Mediated mRNA Translation

| PRJNA1285328 | ENA

Immune checkpoint blockade reprograms systemic immune landscape and tumor microenvironment in obesity-associated breast cancer [tumor]

Project description:Immune checkpoint blockade reprograms systemic immune landscape and tumor microenvironment in obesity-associated breast cancer [tumor]

| PRJNA728069 | ENA

Epigenetic reprogramming shapes the cellular landscape of schwannoma

Project description:Cell state evolution underlies tumor development and response to therapy1, but mechanisms specifying cancer cell states and intratumor heterogeneity are incompletely understood. Schwannomas are the most common tumors of the peripheral nervous system and are treated with surgery and ionizing radiation2–5. Schwannomas can oscillate in size for many years after radiotherapy6,7, suggesting treatment may reprogram schwannoma cells or the tumor microenvironment. Here we show epigenetic reprogramming shapes the cellular landscape of schwannomas. We find schwannomas are comprised of 2 molecular groups distinguished by reactivation of neural crest development pathways or misactivation of nerve injury mechanisms that specify cancer cell states and the architecture of the tumor immune microenvironment. Schwannoma molecular groups can arise independently, but ionizing radiation is sufficient for epigenetic reprogramming of neural crest to immune-enriched schwannoma by remodeling chromatin accessibility, gene expression, and metabolism to drive schwannoma cell state evolution and immune cell infiltration. To define functional genomic mechanisms underlying epigenetic reprograming of schwannomas, we develop a technique for simultaneous interrogation of chromatin accessibility and gene expression coupled with genetic and therapeutic perturbations in single-nuclei. Our results elucidate a framework for understanding epigenetic drivers of cancer evolution and establish a paradigm of epigenetic reprograming of cancer in response to radiotherapy.

2023-04-18 | PXD014798 | Pride

Comprehensive Immune-landscape in Localized Colorectal Cancer

Project description:Surgery still remains the mainstay of treatment for localized colorectal cancer. However, nearly 30% of patients with localized colorectal cancer (stage II and stage III) will present with recurrence. Tumor progression is mediated by both intrinsic genetic changes and by extrinsic epigenetic and host environmental factors, including interactions with the immune system. Several studies demonstrated that tumor infiltrating memory T-cells and type, density and location of infiltrating T cells are better predictors of disease-free survival in patients with CRC compared to the standard TNM staging. These data suggest that tumor invasion and progression are more accurately predicted by immune response in the primary tumor. In addition, mismatch repair (MMR)-deficient tumors are characterized a priori by a higher frequency of tumor infiltrating lymphocytes and are associated with significantly improved prognosis. Recently, Stotz et al showed that the preoperative lymphocyte to monocyte ratio in peripheral blood samples predicts clinical outcome in patients with stage III colon cancer. So far there is no comprehensive analysis of the immune-landscape in CRC. The aim of the current project is to identify a comprehensive panel of immunomarkers in localized colorectal cancer (stage II and stage III) applicable for the detection of patients at high risk of recurrence. For the first time, specific tumor-infiltrating immune cells, mismatch repair protein expression in tumor tissue and preoperative blood based inflammatory markers from routine blood counts in corresponding peripheral blood samples and known clinicopathological features will be correlated with outcome in 300 localized CRC patients.

| 2166592 | ecrin-mdr-crc

Immune checkpoint blockade reprograms systemic immune landscape and tumor microenvironment in obesity-associated breast cancer

Project description:Immune checkpoint blockade reprograms systemic immune landscape and tumor microenvironment in obesity-associated breast cancer

| PRJNA728064 | ENA

Study of human macrophage reprogramming toward a pro-resolving profile by efferocytosis

Project description:Inﬂammation is a physiopathological process triggered by infection or tissue damage. Immune system initiates coordinated sequential steps in response to these danger signals. Once the threat has been contained inflammation has to be subsequently shut down. Inflammation resolution is initiated by the reprogramming of pro-inflammatory macrophages toward a pro-resolving profile. This reprogramming is induced in particular by the non-phlogistic engulfment of apoptotic cells, mostly apoptotic neutrophils, a process called efferocytosis. As a matter of fact, macrophages are an essential linchpin regulating both inflammation triggering and sustaining and inflammation resolution. This duality can be achieved through the tremendous plasticity of these innate immune cells. Indeed, depending on microenvironmental signals (cytokines, efferocytosis, growth factors…) macrophages can adopt numerous diverse and sometimes antagonistic phenotypes. The mechanisms governing these transitions remain relatively scattered especially in human. With this project we propose to explore the mechanisms involved in human macrophage reprogramming toward a pro-resolving profile after efferocytosis. The stakes are high due to the estimated prevalence of chronic inflammatory diseases in Western society is 5 to 7%. Chronic inflammation is a burden to patient due to life-long debilitating illness and increased mortality and is also a burden to society due to high costs for therapy and care. Finding new therapies to limit chronic inflammation establishment and persistence is thus a highly valuable goal.

2021-12-01 | E-MTAB-8885 | biostudies-arrayexpress

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