Research demonstrates that radiotherapy frequently induces immunosuppressive myeloid cells, which drive therapeutic resistance and tumor progression. When radiation is administered, it triggers a p53-TET2 axis that oxidizes methylcytosine marks on chromatin-associated RNAs, leading to chromatin compaction and the suppression of crucial interferon pathways. Conversely, the genetic deletion or pharmacological inhibition of TET2 prevents this suppressive cascade, preserving chromatin accessibility and shifting monocyte differentiation toward immunostimulatory myeloid-derived activating cells. These activating cells successfully restore cytotoxic CD8+ T cell immunity and significantly enhance the efficacy of combined radiotherapy and immunotherapy. Ultimately, targeting this epigenetic pathway offers a promising therapeutic strategy to overcome treatment resistance and suppress metastatic spread.
References:
Ji F, Zheng L, Chen D, et al. Myeloid reprogramming generates myeloid-derived activating cells to potentiate radiotherapy and suppress metastasis[J]. Cancer Cell, 2026.
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