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<p>Glioblastoma therapy remains constrained by a&#xa0;highly interactive tumor microenvironment (TME) that stimulates invasion, resistance, and immune suppression. The glioblastoma TME comprises malignant astrocytic and stem-like tumor cells, resident microglia, infiltrating immune cells, endothelial cells, and a&#xa0;modified extracellular matrix (ECM) that together establish an immunosuppressive tumor stroma. Communication among these elements proceeds through cytokines, chemokines, growth factors, extracellular vesicles, metabolic exchange, and direct cell–matrix contacts. These interactions modulate DNA damage responses (DDRs); remodel immune responses by immunosuppressive and antitumor immune cells; alter the activity of stromal cells; and change angiogenesis, metastasis, and cell survival pathways—which in turn induce resistance to chemo-/radiotherapy. Chemotherapy and radiotherapy induce acute and chronic changes in the TME, including the recruitment of immunosuppressive cells, upregulation of survival signaling in perivascular niches, vascular remodeling, and hypoxia/metabolism rewiring that diminishes the efficacy of chemo-/radiotherapy. Preclinical and early clinical interventions show that targeting cells and their secretions in the TME can be suggested for reprogramming the glioblastoma TME and the subsequent resistance to chemo-/radiotherapy. The focus of this review is to provide mechanistic evidence linking TME communication networks to chemo-/radiotherapy resistance. Strategies that target these interactions to identify translational pathways for combination therapies are reviewed.</p>

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Interactions and communications in the glioblastoma microenvironment: potential targets for chemo-/radiotherapy

  • 期刊论文

  • 发表日期：

    2026年4月22日

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  • Qamar Abuhassan,
  • Hamzeh J. Al-Ameer,
  • Subbulakshmi Ganesan,
  • Priya Priyadarshini Nayak,
  • V. Ramesh Kumar,
  • Vipasha Sharma,
  • Ashish Singh Chauhan,
  • Nargiza Goyibova

摘要

Glioblastoma therapy remains constrained by a highly interactive tumor microenvironment (TME) that stimulates invasion, resistance, and immune suppression. The glioblastoma TME comprises malignant astrocytic and stem-like tumor cells, resident microglia, infiltrating immune cells, endothelial cells, and a modified extracellular matrix (ECM) that together establish an immunosuppressive tumor stroma. Communication among these elements proceeds through cytokines, chemokines, growth factors, extracellular vesicles, metabolic exchange, and direct cell–matrix contacts. These interactions modulate DNA damage responses (DDRs); remodel immune responses by immunosuppressive and antitumor immune cells; alter the activity of stromal cells; and change angiogenesis, metastasis, and cell survival pathways—which in turn induce resistance to chemo-/radiotherapy. Chemotherapy and radiotherapy induce acute and chronic changes in the TME, including the recruitment of immunosuppressive cells, upregulation of survival signaling in perivascular niches, vascular remodeling, and hypoxia/metabolism rewiring that diminishes the efficacy of chemo-/radiotherapy. Preclinical and early clinical interventions show that targeting cells and their secretions in the TME can be suggested for reprogramming the glioblastoma TME and the subsequent resistance to chemo-/radiotherapy. The focus of this review is to provide mechanistic evidence linking TME communication networks to chemo-/radiotherapy resistance. Strategies that target these interactions to identify translational pathways for combination therapies are reviewed.