Introduction: Radioactive iodine (RAI) use is well established in the treatment of differentiated thyroid cancers (DTC). However, the cellular mechanisms by which RAI exerts its cytotoxic effects are still unclear. The p53 gene is known to have a pivotal role in cell death following ionising radiation. Unlike in other cancers, p53 mutation is not required for the initiation of tumorgenesis in DTC. This review aims to determine the p53 dependent and independent pathways of cell death in response to radioiodine in thyroid cells. Elucidation these mechanisms will enable future development of new molecularly targeted therapies to improve the efficacy of radioiodine treatment.
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