Radiation-Induced Thyroid Cancer

Radiation is one of the few accepted risk factors for thyroid cancer. The majority of radiation-induced thyroid carcinomas are well-differentiated papillary carcinomas. Children treated with X-rays for various benign conditions were found to be at increased risk of developing thyroid cancer. Likewise, survivors of the atomic bomb exposures in Hiroshima and Nagasaki, Japan, who were under age 20 at the moment of exposure, were at increased risk of developing thyroid cancer. Latency periods are typically ten or more years, and it appears that excess risk persists for decades after exposure. A pooled analysis of seven major studies over a wide range of doses demonstrated an excess relative risk (ERR) of 7.7 per Gy. In individuals exposed before age 15, linear models best describe the dose–response relationship. Without question, the Chernobyl accident was the worst technological disaster in the history of nuclear power generation. Analysis of post-Chernobyl thyroid carcinomas has demonstrated conclusively that 131I is a thyroid carcinogen in children and adolescents. A linear dose–response relationship has also been documented in children exposed to Chernobyl fallout, with an ERR of 5.25 per Gy after one decade. Molecular analyses have revealed that the mechanism of Chernobyl radiation-induced papillary thyroid cancer pathogenesis is primarily related to double-stranded DNA breaks leading to chromosomal translocations and/or inversions and gene rearrangements. The ret/PTC3 rearrangement was most common in early (prior to 10 years) post-Chernobyl papillary thyroid carcinomas, whereas ret/PTC1 was more common after a 10-year latency period.