Radiation is a carcinogen, interacting with DNA to produce a range of mutations. 
Irradiated cells also show genomic instability, as do adjacent non-irradiated 
cells (the bystander effect); the importance to carcinogenesis remains to be 
established. Current knowledge of radiation effects is largely dependent on 
evidence from exposure to atomic bomb whole body radiation, leading to increases 
in a wide range of malignancies. In contrast, millions of people were exposed to 
radioactive isotopes in the fallout from the Chernobyl accident, within the 
first 20 years there was a large increase in thyroid carcinoma incidence and a 
possible radiation-related increase in breast cancer, but as yet there is no 
general increase in malignancies. The increase in thyroid carcinoma, 
attributable to the very large amounts of iodine 131 released, was first noticed 
in children with a strong relationship between young age at exposure and risk of 
developing papillary thyroid carcinoma (PTC). The extent of the increase, the 
reasons for the relationship to age at exposure, the reduction in attributable 
fraction with increasing latency and the role of environmental factors are 
discussed. The large number of radiation-induced PTCs has allowed new 
observations. The subtype and molecular findings change with latency; most early 
cases were solid PTCs with RET-PTC3 rearrangements, later cases were classical 
PTCs with RET-PTC1 rearrangements. Small numbers of many other RET 
rearrangements have occurred in 'Chernobyl' PTCs, and also rearrangement of 
BRAF. Five of the N-terminal genes found in papillary carcinoma rearrangements 
are also involved in rearrangements in hematological malignancies; three are 
putative tumor suppressor genes, and two are further genes fused to RET in PTCs. 
Radiation causes double-strand breaks; the rearrangements common in these 
radiation-induced tumors reflect their etiology. It is suggested that oncogenic 
rearrangements may commonly involve both a tumor-suppressor gene (or a DNA 
repair gene) as well as an oncogene. Involvement of two relevant genes would 
give a greater chance of progression and a shorter latency than a single-gene 
mutation. More information is needed on germline mutations conferring 
susceptibility to radiation-induced PTCs, particularly DNA repair genes. The 
radiation exposure to the fallout after Chernobyl was very different from the 
whole body radiation after the atomic bombs. The type and molecular pathology of 
the thyroid tumors is changing with increasing latency, long latency tumors in 
other organs could occur in the future. A comprehensive follow up must continue 
for the lifetime of those exposed.