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Changes in the tumor microenvironment and outcome for TME-targeting therapy in glioblastoma: A pilot study

Sehar Ali1, Thaiz F Borin1, Raziye Piranlioglu1

  • 1Laboratory of Tumor Angiogenesis Initiative, Georgia Cancer Center, Augusta University, Augusta, Georgia, United States of America.

Plos One
|February 5, 2021
PubMed

Insights

Targeting the tumor microenvironment (TME) in glioblastoma (GBM) is crucial. TME-targeting therapy improved survival by altering immune cell populations, suggesting sequential treatment strategies for GBM.

Area of Science:

  • Neuro-oncology
  • Immunology
  • Cancer Biology

Background:

  • Glioblastoma (GBM) is an aggressive brain tumor characterized by hypervascularity.
  • Traditional and antiangiogenic therapies often fail due to treatment resistance and tumor recurrence.
  • Alterations in the tumor microenvironment (TME) cellular and metabolic composition are implicated in GBM progression.

Purpose of the Study:

  • To investigate the impact of different therapeutic agents on T-cell populations, macrophage polarization (M1/M2), and myeloid-derived suppressor cells (MDSCs) within the GBM TME.
  • To evaluate the efficacy of TME-targeting therapy in improving tumor growth control and animal survival in a syngeneic GBM model.
  • To hypothesize that TME-associated cell composition varies with therapeutic agents, and TME-targeting therapy can reduce GBM recurrence and enhance survival.

Main Methods:

  • Utilized a syngeneic glioblastoma model to assess changes in TME-associated immune cells.
  • Analyzed T-cell populations, M1/M2 macrophage polarization, and MDSC levels following various treatments.
  • Monitored tumor growth and animal survival rates across different therapeutic groups.

Main Results:

  • Observed that alterations in TME-associated immune cells were dependent on the specific therapeutic agents used.
  • Demonstrated that TME-targeting therapy significantly improved survival rates in animals bearing GBM.
  • Identified that therapeutic strategies influence the composition of immune cells within the tumor microenvironment.

Conclusions:

  • Current GBM therapies require revision to incorporate strategies that prevent the accumulation of immunosuppressive myeloid cells in the TME.
  • Targeting TME-associated cells can counteract mechanisms driving GBM recurrence, such as alternative neovascularization and glioma stem cell revival.
  • A sequential therapeutic approach, rather than concurrent therapy, may be more effective for targeting TME-associated cells in GBM treatment.

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