Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Myeloid-derived suppressor cell subsets drive glioblastoma growth in a sex-specific manner

ABSTRACT: Myeloid-derived suppressor cell subsets drive glioblastoma growth in a sex-specific manner

PROVIDER: PRJNA624324 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11523543_1.fastq.gz	Fastqsanger.gz
	SRR11523543_2.fastq.gz	Fastqsanger.gz
	SRR11523544_1.fastq.gz	Fastqsanger.gz
	SRR11523544_2.fastq.gz	Fastqsanger.gz
	SRR11523545_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 36

Similar Datasets

Myeloid-Derived Suppressor Cell Subsets Drive Glioblastoma Growth in a Sex-Specific Manner.

Project description:Myeloid-derived suppressor cells (MDSC) that block antitumor immunity are elevated in glioblastoma (GBM) patient blood and tumors. However, the distinct contributions of monocytic (mMDSC) versus granulocytic (gMDSC) subsets have yet to be determined. In mouse models of GBM, we observed that mMDSCs were enriched in the male tumors, whereas gMDSCs were elevated in the blood of females. Depletion of gMDSCs extended survival only in female mice. Using gene-expression signatures coupled with network medicine analysis, we demonstrated in preclinical models that mMDSCs could be targeted with antiproliferative agents in males, whereas gMDSC function could be inhibited by IL1β blockade in females. Analysis of patient data confirmed that proliferating mMDSCs were predominant in male tumors and that a high gMDSC/IL1β gene signature correlated with poor prognosis in female patients. These findings demonstrate that MDSC subsets differentially drive immune suppression in a sex-specific manner and can be leveraged for therapeutic intervention in GBM. SIGNIFICANCE: Sexual dimorphism at the level of MDSC subset prevalence, localization, and gene-expression profile constitutes a therapeutic opportunity. Our results indicate that chemotherapy can be used to target mMDSCs in males, whereas IL1 pathway inhibitors can provide benefit to females via inhibition of gMDSCs.See related commentary by Gabrilovich et al., p. 1100.This article is highlighted in the In This Issue feature, p. 1079.

| S-EPMC7415660 | biostudies-literature

Myeloid-derived suppressor cell subsets drive glioblastoma growth in a sex-specific manner

Project description:We report that monocytic (mMDSC) and granulocytic (gMDSC) MDSC susbsets have distinct expression profiles with ~300-1200 genes uniquely expressed on each subset. We further used these genes for pathway annotation. Our findings identified that mMDSC and gMDSC have unique pathway associations that can be targeted via distinct drug candidates.

2020-04-11 | GSE148467 | GEO

Distinct cell adhesion signature defines glioblastoma myeloid-derived suppressor cell subsets

Project description:Distinct cell adhesion signature defines glioblastoma myeloid-derived suppressor cell subsets

| PRJNA851367 | ENA

Distinct cell adhesion signature defines glioblastoma myeloid-derived suppressor cell subsets

Project description:Increased myeloid-derived suppressor cell (MDSC) frequency is associated with worse outcomes and poor therapeutic response in multiple types of cancer. In the glioblastoma (GBM) microenvironment, monocytic (m) MDSCs represent the predominant subset. However, the molecular basis of mMDSC enrichment in the tumor microenvironment compared to granulocytic (g) MDSCs has yet to be determined. Here we performed first broad epigenetic profiling of MDSC subsets to define underlying cell-intrinsic differences in their behavior and found that mMDSCs and gMDSCs display differences in their tumor-accelerating ability, with mMDSCs driving tumor growth in GBM models. Epigenetic assessments revealed enhanced gene accessibility for cell adhesion programs in mMDSCs and higher integrin b1 expression and function in mouse and human mMDSCs. Integrin b1 blockage abrogated the tumor-promoting phenotype of mMDSCs and altered the immune profile in the tumor microenvironment. These findings suggest that integrin b1 expression underlies the enrichment of mMDSCs in tumors and represents a putative immunotherapy target to attenuate myeloid cell-driven immune suppression in GBM.

2022-06-26 | GSE206551 | GEO

Pathologically distinct fibroblast subsets drive inflammation and tissue damage in arthritis

Project description:Pathologically distinct fibroblast subsets drive inflammation and tissue damage in arthritis

| PRJNA530021 | ENA

Pathologically distinct fibroblast subsets drive inflammation and tissue damage in arthritis

Project description:Pathologically distinct fibroblast subsets drive inflammation and tissue damage in arthritis

| PRJNA531402 | ENA

Methylglyoxal-derived nucleoside adducts drive vascular dysfunction in a RAGE-dependent manner

Project description:Methylglyoxal-derived nucleoside adducts drive vascular dysfunction in a RAGE-dependent manner

| PRJNA1055005 | ENA

Brd4-bound enhancers drive cell intrinsic sex differences in glioblastoma.

Project description:Brd4-bound enhancers drive cell intrinsic sex differences in glioblastoma.

| PRJNA658688 | ENA

Brd4-bound enhancers drive cell intrinsic sex differences in glioblastoma

Project description:Brd4-bound enhancers drive cell intrinsic sex differences in glioblastoma

| PRJNA659250 | ENA

Distinct Cell Adhesion Signature Defines Glioblastoma Myeloid-Derived Suppressor Cell Subsets.

Project description:In multiple types of cancer, an increased frequency in myeloid-derived suppressor cells (MDSC) is associated with worse outcomes and poor therapeutic response. In the glioblastoma (GBM) microenvironment, monocytic (m) MDSCs represent the predominant subset. However, the molecular basis of mMDSC enrichment in the tumor microenvironment compared with granulocytic (g) MDSCs has yet to be determined. Here we performed the first broad epigenetic profiling of MDSC subsets to define underlying cell-intrinsic differences in behavior and found that enhanced gene accessibility of cell adhesion programs in mMDSCs is linked to their tumor-accelerating ability in GBM models upon adoptive transfer. Mouse and human mMDSCs expressed higher levels of integrin β1 and dipeptidyl peptidase-4 (DPP-4) compared with gMDSCs as part of an enhanced cell adhesion signature. Integrin β1 blockade abrogated the tumor-promoting phenotype of mMDSCs and altered the immune profile in the tumor microenvironment, whereas treatment with a DPP-4 inhibitor extended survival in preclinical GBM models. Targeting DPP-4 in mMDSCs reduced pERK signaling and their migration towards tumor cells. These findings uncover a fundamental difference in the molecular basis of MDSC subsets and suggest that integrin β1 and DPP-4 represent putative immunotherapy targets to attenuate myeloid cell-driven immune suppression in GBM.SignificanceEpigenetic profiling uncovers cell adhesion programming as a regulator of the tumor-promoting functions of monocytic myeloid-derived suppressor cells in glioblastoma, identifying therapeutic targets that modulate the immune response and suppress tumor growth.

| S-EPMC9664137 | biostudies-literature

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