ReviewCell stress2019
Metabolic and functional reprogramming of myeloid-derived suppressor cells and their therapeutic control in glioblastoma.
Review in Cell stress, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
63 citing papers in PubMed.
- EFEMP2 Is Associated with Shelterin-Related DNA Damage Repair, Immune Microenvironment Features, and Prognosis in Glioblastoma.Biomedicines · 2026Article
- Focused ultrasound for enhancing cell-based immunotherapies in neuro-oncology.Neuro-oncology advances · 2026Review
- Prognostic relevance and cytokine correlates of peripheral immune subpopulations in newly diagnosed glioblastoma.Journal of neuro-oncology · 2026Article
- Disrupting PDGFRA-driven immune evasion in glioma: vaccine-based strategies on the horizon.Frontiers in oncology · 2026Review
- The immunosuppressive tumor microenvironment in glioblastoma.Frontiers in immunology · 2026Review
- Glioblastoma insights: Focus on crosstalk with the suppressive tumor microenvironment and advanced therapeutic strategies.Medicine · 2025Review
- Exploring the Tumor Microenvironment in Osteosarcoma: Driver of Resistance and Progression.Cancers · 2025Review
- Within and beyond the tumor: Mechanisms of glioblastoma-induced immunosuppression.Neuro-oncology advances · 2025Review
- An oxidative stress related gene signature predicts prognosis in cholangiocarcinoma.Discover oncology · 2025Article
- Exploring the tumor microenvironment in diffuse intrinsic pontine glioma: immunological insights and therapeutic challenges.Journal for immunotherapy of cancer · 2025Review
- Insights of immune cell heterogeneity, tumor-initiated subtype transformation, drug resistance, treatment and detecting technologies in glioma microenvironment.Journal of advanced research · 2025Review
- Review
- Immune Cell Interplay in the Fight Against GBM.Cancers · 2025Review
- Tumor secretome shapes the immune landscape during cancer progression.Journal of experimental & clinical cancer research : CR · 2025Review
- Despicable role of epithelial-mesenchymal transition in breast cancer metastasis: ExhibitingCancer pathogenesis and therapy · 2025Review
- Overcoming immunotherapy resistance in glioblastoma: challenges and emerging strategies.Frontiers in pharmacology · 2025Review
- Research progress and challenges of the PD-1/PD-L1 axis in gliomas.Cell & bioscience · 2024Review
- Metabolic Reprogramming in Glioblastoma Multiforme: A Review of Pathways and Therapeutic Targets.Cells · 2024Review
- Review
- Gut microbiota's role in glioblastoma risk, with a focus on the mediating role of metabolites.Frontiers in neurology · 2024Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Glioblastoma, also known as glioblastoma multi-forme, is the most common and deadliest form of high-grade malignant brain tumors with limited available treatments. Within the glioblastoma tumor microenvironment (TME), tumor cells, stromal cells, and infiltrating immune cells continuously interact and exchange signals through various secreted factors including cytokines, chemokines, growth factors, and metabolites. Simultaneously, they dynamically reprogram their metabolism according to environmental energy demands such as hypoxia and neo-vascularization. Such metabolic re-programming can determine fates and functions of tumor cells as well as immune cells. Ultimately, glioma cells in the TME transform immune cells to suppress anti-tumor immune cells such as T, natural killer (NK) cells, and dendritic cells (DC), and evade immune surveillance, and even to promote angiogenesis and tumor metastasis. Glioma-associated microglia/macrophages (GAMM) and myeloid-derived suppressor cells (MDSC) are most abundantly recruited and expanded myeloid lineage cells in glioblastoma TME and mainly lead to immunosuppression. In this review, of myeloid cells we will focus on MDSC as an important driver to induce immunosuppression in glioblastoma. Here, we review current literature on immunosuppressive functions and metabolic reprogramming of MDSCs in glioblastoma and discuss their metabolic pathways as potential therapeutic targets to improve current incurable glioblastoma treatment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.