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Therapeutic potential of targeting macrophages and microglia in glioblastoma
Fei Zhou1, Pritha Mukherjee1, Jinming Mu1
1Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Abstract:
Glioblastoma (GBM) is a highly aggressive and lethal form of brain tumor in human adults that resists standard of care (SOC) and immunotherapy. Tumor-associated macrophages and microglia (TAMs) represent the most abundant cell population within the GBM tumor microenvironment (TME), comprising up to 50% of the whole tumor mass. TAMs play a pivotal role in promoting tumor progression, driving immunosuppression and inducing therapy resistance. Recent advances have revealed TAM heterogeneity - including their cellular identity (e.g., bone marrow-derived macrophages versus microglia) and the presence of distinct activation/function states and subpopulations within each subtype - in GBM tumors. Targeting the context-dependent TAM infiltration, reprogramming, new subpopulations, survival, phagocytosis, and their interactions with GBM cells in the TME has emerged as a promising therapeutic strategy. Herein we review recent advances in pharmacological targeting of the TAM biology and highlight how these strategies may enhance the effectiveness of SOC and immunotherapies in GBM.
Insights
Targeting tumor-associated macrophages (TAMs) in glioblastoma (GBM) offers a promising strategy. Modulating TAMs could overcome resistance to standard care and immunotherapy, improving patient outcomes for this aggressive brain cancer.
Area of Science:
- Neuro-oncology
- Immunology
- Cancer Biology
Background:
- Glioblastoma (GBM) is an aggressive adult brain tumor resistant to current treatments.
- Tumor-associated macrophages and microglia (TAMs) are the most abundant cells in the GBM tumor microenvironment (TME), promoting tumor growth and therapy resistance.
Purpose of the Study:
- To review recent advances in targeting TAM biology in GBM.
- To explore how targeting TAMs can enhance standard of care (SOC) and immunotherapy efficacy.
Main Methods:
- Literature review of recent research on TAMs in GBM.
- Analysis of TAM heterogeneity, including cellular identity and subpopulations.
- Examination of TAM functions: infiltration, reprogramming, survival, and phagocytosis.
Main Results:
- TAMs significantly influence GBM progression, immunosuppression, and treatment resistance.
- TAMs exhibit considerable heterogeneity within the GBM TME.
- Targeting TAMs presents a viable therapeutic avenue.
Conclusions:
- Targeting TAM infiltration, reprogramming, and interactions within the TME is a promising strategy for GBM.
- Pharmacological modulation of TAM biology may improve GBM treatment outcomes.
- Further research into TAM-targeting strategies is warranted to enhance SOC and immunotherapy effectiveness.
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