Modeling Malignant Progression in Glioma
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA767071 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16105400_1.fastq.gz | Fastqsanger.gz | |||
| SRR16105400_2.fastq.gz | Fastqsanger.gz | |||
| SRR16105500_1.fastq.gz | Fastqsanger.gz | |||
| SRR16105500_2.fastq.gz | Fastqsanger.gz | |||
| SRR16105401_1.fastq.gz | Fastqsanger.gz |
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Project description:Modeling Malignant Progression in Glioma
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Project description:Modeling Malignant Progression in Glioma
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Project description:Gliomas are the most common primary brain tumor in humans. Low-grade gliomas (WHO grade II) invariably progress to high-grade gliomas (WHO grade III or IV). Although malignant progression may take many years, the survival rate after transformation to a high-grade glioma is poor, often only 12-15 months. In this data set, we have identified low-grade gliomas that have progressed to high-grade gliomas or high-grade gliomas that have progressed from low-grade gliomas. Some cases are matched pairs (meaning we have both the original low-grade tumor and the subsequent high-grade tumor). The samples deposited have been analyzed with bulk-RNA sequencing. They are also de-identified but are clinically annotated. When available, genetic information including IDH mutation status, 1p/19q deletion and histological subtype are also included.
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Project description:Malignant gliomas are progressive brain cancers with poor prognosis. Pro-tumorigenic glioma associated macrophages (GAM) have been implicated in disease progression however identification of pathogenic functional subsets is lacking. Macrophage functional specification is driven by transcription factor-associated gene regulatory networks, yet the core regulatory transcription factors that govern GAM functions remain unclear. Here we apply single cell RNA/ATAC sequencing to derive the imprint of the glioma tumor microenvironment on GAM transcriptional program specification and identify cell surface markers to prospectively isolate a functionally distinct subpopulation of GAMs in human samples present high grade tumors irrespective of IDH mutation status. This subset of GAMs, termed malignancy associated GAMs (mGAMs) spatially localize to hypoxic metabolic niches and possess a multitude of pro-tumorigenic functions. mGAMs also share somatic mutations with monocytes, suggesting a common bone marrow origin. mGAMs therefore represent a functional subset of GAMs in humans and a potential therapeutic target.
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Project description:Malignant gliomas are progressive brain cancers with poor prognosis. Pro-tumorigenic glioma associated macrophages (GAM) have been implicated in disease progression however identification of pathogenic functional subsets is lacking. Macrophage functional specification is driven by transcription factor-associated gene regulatory networks, yet the core regulatory transcription factors that govern GAM functions remain unclear. Here we apply single cell RNA/ATAC sequencing to derive the imprint of the glioma tumor microenvironment on GAM transcriptional program specification and identify cell surface markers to prospectively isolate a functionally distinct subpopulation of GAMs in human samples present high grade tumors irrespective of IDH mutation status. This subset of GAMs, termed malignancy associated GAMs (mGAMs) spatially localize to hypoxic metabolic niches and possess a multitude of pro-tumorigenic functions. mGAMs also share somatic mutations with monocytes, suggesting a common bone marrow origin. mGAMs therefore represent a functional subset of GAMs in humans and a potential therapeutic target.
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Project description:Malignant gliomas are progressive brain cancers with poor prognosis. Pro-tumorigenic glioma associated macrophages (GAM) have been implicated in disease progression however identification of pathogenic functional subsets is lacking. Macrophage functional specification is driven by transcription factor-associated gene regulatory networks, yet the core regulatory transcription factors that govern GAM functions remain unclear. Here we apply single cell RNA/ATAC sequencing to derive the imprint of the glioma tumor microenvironment on GAM transcriptional program specification and identify cell surface markers to prospectively isolate a functionally distinct subpopulation of GAMs in human samples present high grade tumors irrespective of IDH mutation status. This subset of GAMs, termed malignancy associated GAMs (mGAMs) spatially localize to hypoxic metabolic niches and possess a multitude of pro-tumorigenic functions. mGAMs also share somatic mutations with monocytes, suggesting a common bone marrow origin. mGAMs therefore represent a functional subset of GAMs in humans and a potential therapeutic target.
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Project description:Low grade gliomas (LGG) account for about two-thirds of all glioma diagnoses in adolescents and young adults (AYA) and malignant progression of these patients leads to dismal outcomes. Recent studies have shown the importance of the dynamic tumor microenvironment in high-grade gliomas (HGG), yet its role is still poorly understood in low-grade glioma malignant progression. Here, we investigated the heterogeneity of the immune microenvironment using a platelet-derived growth factor (PDGF)-driven RCAS (replication-competent ASLV long terminal repeat with a splice acceptor) glioma model that recapitulates the malignant progression of low to high-grade glioma in humans and also provides a model system to characterize immune cell trafficking and evolution. To illuminate changes in the immune cell landscape during tumor progression, we performed single-cell RNA sequencing on immune cells isolated from animals bearing no tumor (NT), LGG and HGG, with a particular focus on the myeloid cell compartment, which is known to mediate glioma immunosuppression. LGGs demonstrated significantly increased infiltrating T cells, CD4 T cells, CD8 T cells, B cells, and natural killer cells in the tumor microenvironment, whereas HGGs significantly abrogated this infiltration. Our study identified two distinct macrophage clusters in the tumor microenvironment; one cluster appeared to be bone marrow-derived while another was defined by overexpression of Trem2, a known anti-tumor immunity marker in myeloid cell subpopulations. Our data demonstrates that these two distinct macrophage clusters show an immune-activated phenotype (Stat1, Tnf, Cxcl9 and Cxcl10) in LGG which evolves to an immunosuppressive state (Lgals3, Apoc1 and Id2) in HGG that restricts T cell recruitment and activation. We identified CD74 and macrophage migration inhibition factor (MIF) as potential targets for these distinct macrophage populations. Interestingly, these results were mirrored by our analysis of the TCGA dataset, which demonstrated a statistically significant association between CD74 overexpression and decreased overall survival in AYA patients with grade II LGGs. Targeting immunosuppressive myeloid cells and intra-tumoral macrophages within this therapeutic window may ameliorate mechanisms associated with immunosuppression before and during malignant progression.
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Project description:Malignant gliomas are progressive brain cancers with poor prognosis. Pro-tumorigenic glioma associated macrophages (GAM) have been implicated in disease progression however identification of pathogenic functional subsets is lacking. Macrophage functional specification is driven by transcription factor-associated gene regulatory networks, yet the core regulatory transcription factors that govern GAM functions remain unclear. Here we apply single cell RNA/ATAC sequencing to derive the imprint of the glioma tumor microenvironment on GAM transcriptional program specification and identify cell surface markers to prospectively isolate a functionally distinct subpopulation of GAMs in human samples present high grade tumors irrespective of IDH mutation status. This subset of GAMs, termed malignancy associated GAMs (mGAMs) spatially localize to hypoxic metabolic niches and possess a multitude of pro-tumorigenic functions. mGAMs also share somatic mutations with monocytes, suggesting a common bone marrow origin. mGAMs therefore represent a functional subset of GAMs in humans and a potential therapeutic target.
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