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Blocking EPO Signaling Eliminates Immune-Resistant Liver Tumors in Mice

New research reveals tumor-derived erythropoietin suppresses immune responses, with combined EPO blockade and anti-PD-1 therapy achieving complete tumor regression in preclinical models.

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Overview

  • Erythropoietin (EPO), long known for its role in red blood cell production, has been identified as a key immunosuppressive factor in tumor microenvironments.
  • In mouse models of liver cancer, blocking EPO signaling converted immune-resistant 'cold' tumors into 'hot' tumors, enabling immune cells to attack the cancer.
  • Combining EPO blockade with anti-PD-1 immunotherapy resulted in complete tumor regression and long-term survival in treated mice, a breakthrough for resistant cancers.
  • Tumor hypoxia was found to drive elevated EPO production, which binds to macrophages and suppresses T-cell activity, creating immune-privileged niches for cancer growth.
  • Researchers are advancing preclinical development of therapies targeting EPO signaling, including selective inhibitors to avoid anemia, with human trials in planning stages.