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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© 2017 Published by Elsevier Inc.
