Hypoxia Potentiates Glioma-Mediated Immunosuppression
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Summary
Hypoxia further enhances GBM-mediated immunosuppression, which can be reversed with therapeutic inhibition of STAT3 and HIF-1α and also helps to reconcile the disparate findings that immune therapeutic approaches can be used successfully in model systems but have yet to achieve generalized successful responses.
- Type
- article
- Published
- 2011-01-20
- Cited by
- 218
- References
- 60
- Access
- Open access
- OpenAlex
- https://openalex.org/W21283755
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:589830
Keywords
Identification (biology), Biology
References
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- Efeitos citotóxicos de resolvinas da série D em glioma murino
- Characteristics of Human Cytomegalovirus specific T-Cells in Glioblastoma Multiforme
- Emerging Immune Therapeutics Targeting Glioblastoma-Mediated Immune Suppression: Dark Before the Dawn
- Increased Oxidative Stress as a Selective Anticancer Therapy
- Regulation of self-renewal in colorectal cancer cell models
- Tumor-Associated Microglia/Macrophages Enhance the Invasion of Glioma Stem-like Cells via TGF-β1 Signaling Pathway
- Role of inflammatory pathway and cells on glioma cell response to chemotherapy
- Hypoxia induces escape from innate immunity in cancer cells via increased expression of ADAM10: role of nitric oxide.
- Intratumor Hypoxia Promotes Immune Tolerance by Inducing Regulatory T Cells via TGF-β1 in Gastric Cancer
- Dynamic Interactions Between Cancer Stem Cells And Their Stromal Partners
- The role of regulatory T-cells in glioma immunology.
- Therapeutic targets in subependymoma.
- Hypoxia‐inducible factors as key regulators of tumor inflammation
- Current status of antiangiogenic therapies for glioblastomas
- The cancer stem cell niche(s): the crosstalk between glioma stem cells and their microenvironment.
- Differential regulation of TGF-β-induced, ALK-5-mediated VEGF release by SMAD2/3 versus SMAD1/5/8 signaling in glioblastoma.
- The cancer stem cell niche: cross talk between cancer stem cells and their microenvironment
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