Context-Dependent Glioblastoma-Macrophage/Microglia Symbiosis and Associated Mechanisms

Wenjing Xuan1, Maciej S Lesniak1, Charles David James1

  • 1Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.

Trends in Immunology
|March 5, 2021
PubMed

Insights

Glioblastoma (GBM) cells and their associated immune cells, glioblastoma-associated macrophages/microglia (GAMs), engage in symbiotic interactions that drive tumor growth. Understanding this GBM-GAM relationship may lead to new treatments for brain tumors.

Area of Science:

  • Neuro-oncology
  • Cancer immunology
  • Tumor microenvironment

Background:

  • Glioblastoma (GBM) is an aggressive primary brain tumor in adults.
  • Tumor-intrinsic alterations in GBM impact the tumor microenvironment (TME).
  • Glioblastoma-associated macrophages/microglia (GAMs) are key immune cells within the GBM TME, comprising up to 50% of tumor cells.

Purpose of the Study:

  • To discuss the reciprocal interactions between GBM cells and GAMs.
  • To explore how genetic alterations in GBM affect GAM biology.
  • To elucidate how GAMs contribute to GBM progression.

Main Methods:

  • Literature review and synthesis of current research on GBM-GAM interactions.
  • Analysis of the impact of genetic alterations in GBM on GAM phenotype and function.
  • Examination of the mechanisms by which GAMs promote GBM growth and progression.

Main Results:

  • GBM cells influence GAM polarization and function.
  • GAMs exhibit pro-tumorigenic activities, including promoting angiogenesis, invasion, and immune suppression.
  • Context-dependent symbiotic interactions between GBM and GAMs are crucial for tumor progression.

Conclusions:

  • Understanding the intricate GBM-GAM symbiosis is essential for deciphering GBM tumorigenesis.
  • Targeting GBM-GAM interactions presents a promising therapeutic strategy for improving patient outcomes.
  • Further research into the molecular basis of this symbiosis could reveal novel treatment targets.