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<p>The roles of eosinophil extracellular traps (EETs) in cancer have not been investigated. This research aims to unearth the association between EETs and clinical outcomes in pan-cancer. From the Cancer Genome Atlas (TCGA) program, a 28-gene EETs score was constructed. Overall, higher EETs scores indicated shorter overall survival. EETs were significantly correlated to various pro-tumor processes, including extracellular matrix remodeling, IL-17 signaling, M2 macrophage polarization, and T<sub>reg</sub> differentiation. Immune suppressive M2 macrophages infiltrated more in the tumor microenvironment (TME), while cytotoxic cells (CD8 T and NK cells) were fewer. EETs-gene expression correlated with multiple T cell co-inhibitors. Target molecules of immune checkpoint inhibitors (ICIs) were not in proximity to the EETs disease module. Drugs against IL-5, IL-5RA, CCL-11 and IL-33 scored highly in perturbation of the disease module. Therefore, the EETs formation was coordinated with the adverse clinical outcomes and TME alternations in cancer. The role of EETs and anti-eosinophil therapy in cancer deserve further investigation in the era of immunotherapy.</p>

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Eosinophil extracellular traps formation is correlated with cancer prognosis by tumor microenvironment remodeling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月17日

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  • Jingdai Zhang,
  • Yu Qiu,
  • Yifan Liu,
  • Shengwei Mo,
  • Muwen Nie,
  • Hui Zhang,
  • Xiaohang Liu,
  • Wei Chen

摘要

The roles of eosinophil extracellular traps (EETs) in cancer have not been investigated. This research aims to unearth the association between EETs and clinical outcomes in pan-cancer. From the Cancer Genome Atlas (TCGA) program, a 28-gene EETs score was constructed. Overall, higher EETs scores indicated shorter overall survival. EETs were significantly correlated to various pro-tumor processes, including extracellular matrix remodeling, IL-17 signaling, M2 macrophage polarization, and Treg differentiation. Immune suppressive M2 macrophages infiltrated more in the tumor microenvironment (TME), while cytotoxic cells (CD8 T and NK cells) were fewer. EETs-gene expression correlated with multiple T cell co-inhibitors. Target molecules of immune checkpoint inhibitors (ICIs) were not in proximity to the EETs disease module. Drugs against IL-5, IL-5RA, CCL-11 and IL-33 scored highly in perturbation of the disease module. Therefore, the EETs formation was coordinated with the adverse clinical outcomes and TME alternations in cancer. The role of EETs and anti-eosinophil therapy in cancer deserve further investigation in the era of immunotherapy.