Secondary Thyroid Cancer after Exposure to Radioactive Iodine from the Fukushima Daiichi Nuclear Power Plant accident
Received Date: Jul 10, 2012 / Accepted Date: Jul 10, 2012 / Published Date: Jul 15, 2012
The catastrophic great east Japan earthquake on March 11, 2011 triggered the explosion of Fukushima Daiichi Nuclear Power Plants. As a result, high volatility fission products including 129mTe, 131I, 134Cs, 136Cs, and 137Cs were released into the air and deposited on the ground. Moreover, highly radioactive contaminated water continued to escape from the nuclear plant after 1 year after the accident. Although the impacts of radiation exposure on rates of non-thyroid solid cancers and leukemia in the exposed population is still unclear, strong evidence of an increased risk of developing secondary thyroid cancer was found among children who were exposed to radioactive iodine after the Chernobyl Nuclear Power Plant accident on 26 April 1986 in Ukraine. Ideally, potassium iodide should be prophylactically administered before or within several hours after 131I exposure. Administration of potassium iodide more than 1 day after exposure has a limited effect and is not recommended unless further exposure is expected . In the case of Fukushima, children were not given prophylactic potassium iodide immediately. Thyroid screening for children who are among the evacuees was started in October 2011 and has gradually increased, and screening for the all citizens who are younger than 18 years will be started in Fukushima prefecture after 2014.
Thyroid screening should be started immediately after a nuclear disaster both for early detection of disease in the affected population and to estimate the incidence of secondary thyroid cancer as accurately as possible. It is difficult to determine the most appropriate level of screening because the efficacy of screening relies on the level (i.e. Screening more people is costly but has limited benefits). Some increase in the reported incidence of secondary thyroid cancer after the Fukushima accident may be observed because of the screening effect, no matter how carefully data are collected. However, even though the screening effect may decrease over time, the eligibility of citizens for screening should not be geographically narrowed considering the scattered hot spots of radioactive agents in prefectures outside of Fukushima. Precise information from individuals and the radiation level in each area should be tracked.
As the number of examined individuals rises, the need for Fine- Needle Aspiration Cytology (FNAC) will increase. The diagnostic accuracy of FNAC reaches more than 95% for papillary thyroid cancer in adolescence, although the diagnostic accuracy of FNAC for follicular cancer is still low. Additionally, increasing the diagnostic accuracy of FNAC in children is very important, as it is increasing the specificity of ultrasound screening.
Other diagnostic and prognostic markers are needed to refine the accuracy of FNAC and to estimate the aggressiveness of each tumor. The revised management guidelines of the American Thyroid Association recommend the use of an appropriate mutational panel for thyroid nodules with indeterminate FNAC to assist clinical management . Most sporadic thyroid cancers are caused by either a point mutation or chromosomal rearrangement. A point mutation is a single nucleotide change, often in the RAS and BRAF genes. Chromosomal rearrangement can be a deletion, duplication, inversion, and translocation, caused by breakage and fusion of parts of chromosomes .
Chromosomal rearrangements of the tyrosine kinase protooncogene RET, specifically RET/PTC rearrangements, are considered a hallmark of radiation-induced thyroid cancer and are found in approximately 80% of patients with papillary thyroid cancer who were exposed to either accidental radiation or therapeutic radiation during childhood or adolescence [4,5]. The two most common types of rearrangements are RET/PTC1 (fusion with CCDC6) and RET/PTC3 (fusion with NCOA4) [6,7]. RET/PTC3 rearrangements was the most common mutation observed after the Chernobyl accident, followed by the RET/PTC1 rearrangements with delay . Indeed, radioactive induction of RET/PTC rearrangements was confirmed by animal and in vitro experiments [9-11]. However, high incidence of RET/ PTC rearrangements is also reported in sporadic childhood papillary thyroid cancer in patients with no history of exposure to radiation . Therefore, discovery of more sensitive and specific markers of thyroid cancer is greatly needed to improve early detection, prognostication, and determination of the most appropriate treatment. It is also important for determination of governmental compensation.
In 2005, nearly 20 years after the Chernobyl accident, researchers finally reached a consensus on the causal relationship of radiation exposure with thyroid cancer. Accumulation of a sufficient number of patients with a disease to show statistical evidence of a cause takes a long time, often resulting in insufficient governmental provision of resources to address the problem. Thus, it is important to pay more attention to individual cases and not to overlook specific signs of a cause that may be proven with more evidence in the future.
Hiroshi Katoh was supported by the Uehara Memorial Foundation Research Fellowship. Makoto Adachi was supported by the Uehara Memorial Foundation Postdoctoral Fellowship and the Japan Society for the Promotion of Science Postdoctoral Fellowship for Research Abroad. None of the study sponsors had any role in the decision to submit this manuscript for publication. We particularly thank the Otolaryngology editorial team.
Conflict of Interest
The authors declare no conflict of interest.
- Zanzonico PB, Becker DV (2000) Effects of time of administration and dietary iodine levels on potassium iodide (KI) blockade of thyroid irradiation by 131I from radioactive fallout. Health Phys 78: 660-667.
- Cooper DS, Doherty GM, Haugen BR, Kloos RT, Lee SL, et al. (2009) Revised American Thyroid Association management guidelines for patients with thyroid nodules and differentiated thyroid cancer. Thyroid 19: 1167-1214.
- Nikiforov YE, Nikiforova MN (2011) Molecular genetics and diagnosis of thyroid cancer. Nat Rev Endocrinol 7: 569-580.
- Bounacer A, Wicker R, Caillou B, Cailleux AF, Sarasin A, et al. (1997) High prevalence of activating ret proto-oncogene rearrangements, in thyroid tumors from patients who had received external radiation. Oncogene 15: 1263-1273.
- Rabes HM, Demidchik EP, Sidorow JD, Lengfelder E, Beimfohr C, et al. (2000) Pattern of radiation-induced RET and NTRK1 rearrangements in 191 post-chernobyl papillary thyroid carcinomas: biological, phenotypic, and clinical implications. Clin Cancer Res 6: 1093-1103.
- Grieco M, Santoro M, Berlingieri MT, Melillo RM, Donghi R, et al. (1990) PTC is a novel rearranged form of the ret proto-oncogene and is frequently detected in vivo in human thyroid papillary carcinomas. Cell 60: 557-563.
- Santoro M, Dathan NA, Berlingieri MT, Bongarzone I, Paulin C, et al. (1994) Molecular characterization of RET/PTC3; a novel rearranged version of the RETproto-oncogene in a human thyroid papillary carcinoma. Oncogene 9: 509-516.
- Trovisco V, Soares P, Preto A, Castro P, Maximo V, et al. (2007) Molecular genetics of papillary thyroid carcinoma: great expectations. Arq Bras Endocrinol Metabol 51: 643-653.
- Caudill CM, Zhu Z, Ciampi R, Stringer JR, Nikiforov YE (2005) Dose-dependent generation of RET/PTC in human thyroid cells after in vitro exposure to gamma-radiation: a model of carcinogenic chromosomal rearrangement induced by ionizing radiation. J Clin Endocrinol Metab 90: 2364-2369.
- Ito T, Seyama T, Iwamoto KS, Hayashi T, Mizuno T, et al. (1993) In vitro irradiation is able to cause RET oncogene rearrangement. Cancer Res 53: 2940-2963.
- Mizuno T, Iwamoto KS, Kyoizumi S, Nagamura H, Shinohara T, et al. (2000) Preferential induction of RET/PTC1 rearrangement by X-ray irradiation. Oncogene 19: 438-443.
Citation: Katoh H, Watanabe M, Adachi M (2012) Secondary Thyroid Cancer after Exposure to Radioactive Iodine from the Fukushima Daiichi Nuclear Power Plant accident. Otolaryngology 2:e104. Doi: 10.4172/2161-119X.1000e104
Copyright: © 2012 Katoh H, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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