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Phenotypic plasticity of myeloid cells in glioblastoma development, progression, and therapeutics

期刊

ONCOGENE
卷 40, 期 42, 页码 6059-6070

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SPRINGERNATURE
DOI: 10.1038/s41388-021-02010-1

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资金

  1. National Natural Science Foundation of China [81822034, 81821002]
  2. National Key Research and Development Program of China [2017YFA0106800, 2018YFA0109200]
  3. Sichuan Science-Technology International Cooperation Project [2019YFH0144]
  4. Sichuan Science-Technology Key Research and Development Program [2021YFS0015]
  5. West China Second Hospital, Sichuan University [KS021, K1907]

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Research suggests that targeting infiltrating myeloid cells in the tumor microenvironment may offer a novel direction for immunotherapy in improving the prognosis of patients with Glioblastoma (GBM). These myeloid cells play a crucial role in regulating GBM progression and affecting therapeutic efficacy.
Glioblastoma (GBM) is the most common and malignant type of intracranial tumors with poor prognosis. Accumulating evidence suggests that phenotypic alterations of infiltrating myeloid cells in the tumor microenvironment are important for GBM progression. Conventional tumor immunotherapy commonly targets T-cells, while innate immunity as a therapeutic target is an emerging field. Targeting infiltrating myeloid cells that induce immune suppression in the TME provides a novel direction to improve the prognosis of patients with GBM. The factors released by tumor cells recruit myeloid cells into tumor bed and reprogram infiltrating myeloid cells into immunostimulatory/immunosuppressive phenotypes. Reciprocally, infiltrating myeloid cells, especially microglia/macrophages, regulate GBM progression and affect therapeutic efficacy. Herein, we revisited biological characteristics and functions of infiltrating myeloid cells and discussed the recent advances in immunotherapies targeting infiltrating myeloid cells in GBM. With an evolving understanding of the complex interactions between infiltrating myeloid cells and tumor cells in the tumor microenvironment, we will expand novel immunotherapeutic regimens targeting infiltrating myeloid cells in GBM treatment and improve the outcomes of GBM patients.

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