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1690-Myeloid Reprogramming to Enhance Radiotherapy

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…

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