Myeloid reprogramming generates myeloid-derived activating cells to potentiate radiotherapy and suppress metastasis.

Inhibiting TET2 reprograms myeloid cells to enhance radiotherapy and suppress metastasis, improving outcomes in lung cancer models.

• Why it matters: Radiation induces immunosuppressive myeloid cells that hinder therapy and promote metastasis, creating a need for strategies to counteract this resistance and improve patient survival.
• What they did: The study used genetic deletion and pharmacological inhibition of TET2 in myeloid cells, combined with radiotherapy and immune checkpoint blockade, to assess effects on tumor progression and immune responses.
• The result: TET2 inhibition redirected myeloid differentiation toward activating cells, boosted T cell cytotoxicity, and significantly improved control of primary and metastatic tumors, suggesting a promising therapeutic approach.