AI Article Synopsis
- Glioblastomas (GBM) are highly aggressive brain tumors associated with poor survival rates, heavily involving immune cells like macrophages and microglia in their tumor microenvironment.
- Tumor-derived extracellular vesicles (EVs) hinder macrophage inflammatory responses, making it harder for these immune cells to recognize and attack cancer cells, while also prompting macrophages to produce EVs that further facilitate tumor growth and spread.
- The review focuses on understanding how GBM EVs alter macrophage functions, the implications of macrophage-derived EVs on tumor progression, and potential therapies aimed at disrupting this harmful interaction.
Article Abstract
Glioblastomas (GBM) are a devastating disease with extremely poor clinical outcomes. Resident (microglia) and infiltrating macrophages are a substantial component of the tumor environment. In GBM and other cancers, tumor-derived extracellular vesicles (EVs) suppress macrophage inflammatory responses, impairing their ability to identify and phagocytose cancerous tissues. Furthermore, these macrophages then begin to produce EVs that support tumor growth and migration. This cross-talk between macrophages/microglia and gliomas is a significant contributor to GBM pathophysiology. Here, we review the mechanisms through which GBM-derived EVs impair macrophage function, how subsequent macrophage-derived EVs support tumor growth, and the current therapeutic approaches to target GBM/macrophage EV crosstalk.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10219523 | PMC |
| http://dx.doi.org/10.3390/jcm12103430 | DOI Listing |
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