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Author Notes:

Correspondence: Zhihong Chen, zhihong.chen@emory.edu; Dolores Hambardzumyan, dhambar@emory.edu

Both ZC and DH contributed to conceive the article, review the literature, and write the manuscript.

We thank Dr. Chris Nelson for editorial assistance and Dr. Selene Virk for contributing to Figure ​Figure2.2. We are also grateful to Mr. Dave Schumick for the illustrations.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Subjects:

Research Funding:

This work is supported by NIH grants U01-CA160882 and R01-NS100864 to DH.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Immunology
  • glioblastoma
  • macrophages
  • microglia
  • immunotherapy
  • tumor-associated macrophages
  • tumor microenvironment
  • REGULATORY T-CELLS
  • MACROPHAGE POLARIZATION
  • INFILTRATING MONOCYTES
  • CHECKPOINT BLOCKADE
  • RESIDENT MICROGLIA
  • MYELOID CELLS
  • GLIOMA
  • EXPRESSION
  • CANCER
  • BRAIN

Immune Microenvironment in Glioblastoma Subtypes

Tools:

Journal Title:

Frontiers in Immunology

Volume:

Volume 9, Number MAY

Publisher:

, Pages 1004-1004

Type of Work:

Article | Final Publisher PDF

Abstract:

Glioblastomas (GBMs) are the most common and aggressive primary brain tumors. Due to their malignant growth and invasion into the brain parenchyma coupled with resistance to therapy, GBMs are among the deadliest of all cancers. GBMs are highly heterogeneous at both the molecular and histological levels. Hallmark histological structures include pseudopalisading necrosis and microvascular proliferation. In addition to high levels of intratumoral heterogeneity, GBMs also exhibit high levels of inter-tumoral heterogeneity. The major non-neoplastic cell population in the GBM microenvironment includes cells of the innate immune system called tumor-associated macrophages (TAMs). Correlative data from the literature suggest that molecularly distinct GBM subtypes exhibit differences in their microenvironment. Data from mouse models of GBM suggest that genetic driver mutations can create unique microenvironments. Here, we review the origin, features, and functions of TAMs in distinct GBM subtypes. We also discuss their interactions with other immune cell constituents and discuss prospects of therapeutically targeting TAMs to increase the efficacy of T-cell functions.

Copyright information:

© 2018 Chen and Hambardzumyan.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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