ReviewFrontiers in immunology2026
Radioiodine-induced cGAS-STING signaling and antitumor immunity in thyroid cancer.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Radioiodine (RAI) is a cornerstone of treatment for differentiated thyroid cancer (DTC), yet the immunological consequences of RAI-induced DNA damage remain poorly understood. Here, we examine cGAS-STING signaling as a potential mechanistic link between RAI-induced genotoxic stress and antitumor immunity. RAI delivers prolonged, thyroid-selective radiation to iodine-avid tumors, providing a plausible source of extranuclear DNA capable of engaging innate DNA sensing. We propose that transient RAI-associated cGAS-STING activation in DTC may favor IRF3-type I interferon-dependent immune priming, whereas persistent genomic stress in RAI-refractory anaplastic and poorly differentiated thyroid cancers (ATC/PDTC) may shift pathway output toward NF-κB-dominated, myeloid-suppressive programs. This acute-versus-chronic framework suggests that cGAS-STING dynamics could help define a therapeutic window for sequencing RAI with immune checkpoint blockade, while controlled STING activation may provide an alternative strategy for iodine-refractory disease. Direct evidence for RAI-induced cGAS-STING activation in thyroid tumors remains lacking, highlighting the need to define pathway kinetics across thyroid cancer subtypes and determine whether thyroid-specific endocrine signaling, including TSH-TSHR signaling, further modulates innate DNA sensing.
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