Mesenchymal Stromal-Like Cells in the Glioma Microenvironment: What Are These Cells?

Clavreul, Anne; Meneï, Philippe

doi:10.3390/cancers12092628

Cited by 19 publications

(19 citation statements)

References 49 publications

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“…The GASC is a recently identified particular type of cell in the glioma microenvironment, with various names, e.g., glioma-associated human MSCs (GA-hMSCs) ( 7 ). The phenotypic and functional properties of GASCs are similar to those of cancer-associated fibroblasts and mesenchymal stem cells.…”

Section: Discussionmentioning

confidence: 99%

“…THY1 (CD90) is a surrogate marker for a variety of stem cells, including glioblastoma stem cells (GSC) ( 31 ) and GASC ( 7 ). Svensson et al detected CD90 - and CD90 + GASC subpopulations by cell sorting and discovered that the CD90 - subpopulation exhibited greater tumor vascularization and immunosuppression activity than the CD90 + subpopulation ( 32 ).…”

Section: Discussionmentioning

confidence: 99%

“…A gene set of GASC markers ( Table S1 ) was obtained from Clavreul et al ( 7 ). Enrichment scores for GASCs were separately calculated for each sample with the Single-sample Gene Set Enrichment Analysis (ssGSEA) algorithm.…”

Section: Methodsmentioning

confidence: 99%

“…THY1 (CD90) is a surrogate marker for a variety of stem cells, including glioblastoma stem cells (GSC) (31) and GASC (7). Svensson GASCs drove glioma progression via increasing proliferation, migration, and adhesion.…”

Section: Mcdonald Et Al Reported That Deletion Of Dr3 (Tumormentioning

confidence: 99%

“…The glioma-associated stromal cell (GASC) is a recently identified important stromal cell in the glioma microenvironment, with potential value for prognostic prediction and therapeutic perspectives ( 7 ). The available evidence indicates that GASCs facilitate angiogenesis, invasion, and tumor growth ( 7 ). However, the potential mechanisms of GASCs remain largely unknown.…”

Section: Introductionmentioning

confidence: 99%

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Glioma-Associated Stromal Cells Stimulate Glioma Malignancy by Regulating the Tumor Immune Microenvironment

et al. 2021

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BackgroundThe glioma-associated stromal cell (GASC) is a recently identified type of cell in the glioma microenvironment and may be a prognostic marker for glioma. However, the potential mechanisms of GASCs in the glioma microenvironment remain largely unknown. In this work, we aimed to explore the mechanisms of GASCs in gliomas, particularly in high-grade gliomas (HGG).MethodsWe used glioma datasets from The Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA). We utilized the Single-sample Gene Set Enrichment Analysis (ssGSEA) algorithm to discriminate between patients with high or low GASC composition. The xCELL and CIBERSORT algorithms were used to analyze the composition of stromal cells and immune cells. Risk score and a nomogram model were constructed for prognostic prediction of glioma.ResultsWe observed for the first time that the levels of M2 macrophages and immune checkpoints (PD-1, PD-L1, PD-L2, TIM3, Galectin-9, CTLA-4, CD80, CD86, CD155, and CIITA) were significantly higher in the high GASC group and showed positive correlation with the GASC score in all glioma population and the HGG population. Copy number variations of DR3 and CIITA were higher in the high-GASC group. THY1, one of the GASC markers, exhibited lower methylation in the high GASC group. The constructed risk score was an independent predictor of glioma prognostics. Finally, a credible nomogram based on the risk score was established.ConclusionsGASCs stimulate glioma malignancy through the M2 macrophage, and are associated with the level of immune checkpoints in the glioma microenvironment. The methylation of THY1 could be used as prognostic indicator and treatment target for glioma. However, further studies are required to verify these findings.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Mcdonald Et Al Reported That Deletion Of Dr3 (Tumormentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Glioma-Associated Stromal Cells Stimulate Glioma Malignancy by Regulating the Tumor Immune Microenvironment

et al. 2021

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Proteomics of tumor and serum samples from isocitrate dehydrogenase‐wildtype glioblastoma patients: is the detoxification of reactive oxygen species associated with shorter survival?

Clavreul,

Guette,

Lasla

et al. 2024

Molecular Oncology

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Proteomics has been little used for the identification of novel prognostic and/or therapeutic markers in isocitrate dehydrogenase (IDH)‐wildtype glioblastoma (GB). In this study, we analyzed 50 tumor and 30 serum samples from short‐ and long‐term survivors of IDH‐wildtype GB (STS and LTS, respectively) by data‐independent acquisition mass spectrometry (DIA‐MS)‐based proteomics, with the aim of identifying such markers. DIA‐MS identified 5422 and 826 normalized proteins in tumor and serum samples, respectively, with only three tumor proteins and 26 serum proteins displaying significant differential expression between the STS and LTS groups. These dysregulated proteins were principally associated with the detoxification of reactive oxygen species (ROS). In particular, GB patients in the STS group had high serum levels of malate dehydrogenase 1 (MDH1) and ribonuclease inhibitor 1 (RNH1) and low tumor levels of fatty acid‐binding protein 7 (FABP7), which may have enabled them to maintain low ROS levels, counteracting the effects of the first‐line treatment with radiotherapy plus concomitant and adjuvant temozolomide. A blood score built on the levels of MDH1 and RNH1 expression was found to be an independent prognostic factor for survival based on the serum proteome data for a cohort of 96 IDH‐wildtype GB patients. This study highlights the utility of circulating MDH1 and RNH1 biomarkers for determining the prognosis of patients with IDH‐wildtype GB. Furthermore, the pathways driven by these biomarkers, and the tumor FABP7 pathway, may constitute promising therapeutic targets for blocking ROS detoxification to overcome resistance to chemoradiotherapy in potential GB STS.

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The peritumoral brain zone in glioblastoma: where we are and where we are going

Giambra

Cristofori

Valtorta

et al. 2022

J of Neuroscience Research

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Glioblastoma (GBM) is the most aggressive and invasive primary brain tumor. Current therapies are not curative, and patients' outcomes remain poor with an overall survival of 20.9 months after surgery. The typical growing pattern of GBM develops by infiltrating the surrounding apparent normal brain tissue within which the recurrence is expected to appear in the majority of cases. Thus, in the last decades, an increased interest has developed to investigate the cellular and molecular interactions between GBM and the peritumoral brain zone (PBZ) bordering the tumor tissue. The aim of this review is to provide up‐to‐date knowledge about the oncogenic properties of the PBZ to highlight possible druggable targets for more effective treatment of GBM by limiting the formation of recurrence, which is almost inevitable in the majority of patients. Starting from the description of the cellular components, passing through the illustration of the molecular profiles, we finally focused on more clinical aspects, represented by imaging and radiological details. The complete picture that emerges from this review could provide new input for future investigations aimed at identifying new effective strategies to eradicate this still incurable tumor.

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Mesenchymal Stromal-Like Cells in the Glioma Microenvironment: What Are These Cells?

Cited by 19 publications

References 49 publications

Glioma-Associated Stromal Cells Stimulate Glioma Malignancy by Regulating the Tumor Immune Microenvironment

Glioma-Associated Stromal Cells Stimulate Glioma Malignancy by Regulating the Tumor Immune Microenvironment

Proteomics of tumor and serum samples from isocitrate dehydrogenase‐wildtype glioblastoma patients: is the detoxification of reactive oxygen species associated with shorter survival?

The peritumoral brain zone in glioblastoma: where we are and where we are going

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