Abstract
Enormous amounts of childhood thyroid cancers, mostly childhood papillary thyroid carcinomas (PTCs), after the Chernobyl nuclear power plant accident have revealed a mutual relationship between the radiation exposure and thyroid cancer development. While the internal exposure to radioactive 131I is involved in the childhood thyroid cancers after the Chernobyl accident, people exposed to the external radiation, such as atomic-bomb (A-bomb) survivors, and the patients who received radiation therapy, have also been epidemiologically demonstrated to develop thyroid cancers. In order to elucidate the mechanisms of radiation-induced carcinogenesis, studies have aimed at defining the molecular changes associated with the thyroid cancer development. Here, we overview the literatures towards the identification of oncogenic alterations, particularly gene rearrangements, and discuss the existence of radiation signatures associated with radiation-induced thyroid cancers.
Highlights
Radiation exposure has been well documented to take part in cancer development in the human body
Subsequent studies have shown that the Rearranged During Transfection (RET)/PTC1 rearrangement is a common type of oncogenic mutation in the childhood thyroid cancers after the Chernobyl accident [28], and the RET/papillary thyroid carcinomas (PTCs) rearrangements are recognized as predominant driver mutations in both radiation-related and sporadic childhood papillary thyroid cancers [29,30]
Molecular analyses in the adult-onset PTC cases have demonstrated that more than half of the exposed patients exhibited the BRAF point mutation (56%), and the RET/PTC rearrangement was observed in 22% of the exposed patients, while more than 80% of the non-exposed cases harbored the BRAF gene point mutation [47]
Summary
Radiation exposure has been well documented to take part in cancer development in the human body. Increased risks in a variety of cancer mortality/incidences, including the thyroid cancer incidence, have been demonstrated among the Life Span Study (LSS) cohort of the A-bomb survivors in Hiroshima and Nagasaki [1,2]. Epidemiological studies have indicated an apparent dose-dependent induction of thyroid cancers, confirming that the radiation exposure is the primary cause of thyroid cancer induction [7,8,9]. Other examples include the increased thyroid cancer incidence in the patients who received medical radiation therapy for diseases, such as tinea capitis, enlarged thymus glands, and tonsils [10]. Radiation-induced thyroid cancers have provided unequalled examples to unveil the molecular mechanisms of radiation-induced carcinogenesis, as well as a role of radiation exposure in thyroid carcinogenesis
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