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The common sources of ionizing radiation exposure to the thyroid gland in humans are accidental environmental exposure and medical, therapeutic, or diagnostic irradiation. Radiation often induces notable histologic changes in the thyroid tissue and is a well-established risk factor for benign and malignant thyroid tumors. In this paper, we review the acute and chronic histologic changes in the thyroid gland subjected to irradiation, and characterize benign thyroid nodules and malignant tumors arising after exposure, with particular emphasis on thyroid lesions in the population exposed to ionizing radiation as a result of the Chernobyl nuclear accident.

Starting 4 years after the Chernobyl accident, a dramatic increase in incidence of thyroid carcinoma was noticed in children from contaminated areas. The incidence of benign thyroid lesions in the exposed population was also increased. To study the possible role of ras and p53 genes in radiation-induced thyroid tumorigenesis, 33 papillary carcinomas, one follicular carcinoma and 22 benign lesions removed from children aged 5-19 were screened for point mutations of H-, K-, and N-ras, as well as of p53 (exons 5-8) using single strand conformation polymorphism (SSCP) analysis. Ras point mutations were detected in 1/1 case of follicular carcinoma (N-ras codon 61 CAAgln-->AAAlys), and in 3/7 follicular adenomas (N-ras codon 61 CAAgln-->CGAarg x 2, CAAgln-->AAAlys). None of the cases of papillary thyroid carcinoma was positive for ras oncogene abnormalities. The lack of K-ras mutations was confirmed by allele-specific oligonucleotide hybridization (ASOH), and by sequencing in five cases. Somatic point mutations in p53 were found by SSCP in 2/33 papillary thyroid carcinomas, with one missense mutation (exon 5, codon 160 ATGmet-->GTGval) and another silent mutation (codon 182, TGCcys-->TGTcys). Immunohisto-chemically, focally positive p53 staining was found in four papillary carcinomas being primarily confined to solid and poorly-differentiated areas in tumors. These data demonstrate that as opposed to the few reports on tumors arising after therapeutic external irradiation, ras mutations are not primary events in the development of post-Chernobyl thyroid papillary carcinomas. p53 mutations do not appear to be important in the development of these tumors, but may in some cases have a role in progression to a more aggressive phenotype that has not yet fully manifested in these pediatric neoplasms.

Eight years after the Chernobyl nuclear accident, the most obvious effect is manifested by an increase in the prevalence of thyroid gland diseases in the exposed children and adolescents. In this study, we describe a comparative analysis of epidemiological, clinical, and morphological features of 92 malignant and 59 benign thyroid lesions from patients 5-18 yr of age exposed to radiation in Belarus as a result of the Chernobyl disaster. All of them were operated at the same institution during the period from September 1991 through December 1992. The highest number of patients that subsequently developed thyroid carcinomas was in the group that was less that 1 yr of age at the time of Chernobyl, and this number decreased progressively through age 12 yr. Conversely, none of the patients with benign lesions only was less than 2 yr old at the time of the accident, and an exposure age of 5-6 yr was a threshold separating significant prevalence of malignant tumors in younger children from the more frequent benign lesions in older patients (P < 0.001). Fifty-two percent of children with carcinomas and only 24% with benign lesions (P < 0.005) were residents of the Gomel region, which is the most contaminated in Belarus. The morphology of thyroid tissue adjacent to carcinomas showed a high prevalence of multinodular and diffuse changes, but not of adenomas or solitary adenomatoid nodules. There was a high prevalence of focal micropapillary hyperplasia with graded degrees of severity, which we hypothesize may correspond to precursors for papillary thyroid carcinoma in post-Chernobyl radiation-associated tumors.

Background: In addition to the previously reported increase in incidence of thyroid carcinomas in Belarussian children after the Chernobyl disaster in April, 1986, benign thyroid lesions were also found to be increased in the exposed population., Methods: A total of 60 follicular neoplasms and benign nonneoplastic thyroid lesions arising after the Chernobyl disaster in children and adolescents of 7 to 18 years of age were studied., Results: The primary diagnoses in this series were follicular carcinoma in 1 (2%) case, follicular adenoma in 9 (15%), cystic adenomatoid nodule with papillae in 18 (30%), multinodular goiter in 18 (30%), diffuse hyperplasia in 2 (3%), diffuse hyperplasia with atypia and nodularity in 5 (8%), lymphocytic thyroiditis in 6 (10%), and thyroid cyst in 1 patient (2%). Additional histologic changes in thyroid glands from these patients were similar to those reported after radiation exposure, and included perifollicular fibrosis (72%), focal epithelial hyperplasia (73%), colloid accumulation (47%), follicular atrophy (33%), and cellular atypia (25%). Vascular abnormalities were found more often (75%) than previously reported in the thyroid gland after irradiation, and had a somewhat different appearance. They affected primarily medium-size arteries and were characterized by damage of the internal elastic lamina in addition to intimal fibrosis., Conclusions: The first case of thyroid follicular carcinoma in the exposed Belarussian children was diagnosed after a latent period of 6.5 years, as compared with 4 years of minimal latency for post-Chernobyl papillary carcinomas. Among benign thyroid lesions, cystic adenomatoid nodules of papillary type and diffuse hyperplasia with cellular atypia and nodularity seem to be commonly associated with radiation exposure to the thyroid gland.