During the past three decades, the deleterious consequences of Chornobyl 
accident including carcinogenic effects in the people who were accidentally 
exposed to radiation have been intensively studied. In particular, recent 
studies provided increased knowledge of the molecular pathogenesis of thyroid 
tumors in children exposed to Chornobyl fallout. The risk of several forms of 
leukemia including myelodysplastic syndromes is elevated in Chornobyl 
liquidators. Furthermore, the upward trends of increases in a variety of other 
tumors including breast cancer, cancers of central nervous system and renal 
cancer have been reported in the persons exposed to Chornobyl fallout. There is 
growing evidence that insufficient apoptosis allows irradiated cells to survive 
and thereby contributes to carcinogenesis. The purpose of the present survey is 
to summarize the recent findings related to apoptotic biomarkers among cancer 
patients from the different populations affected by the Chornobyl catastrophe. 
Among the particularly radiosensitive cancer sites, we focused on thyroid cancer 
and leukemia. Several genes and/or proteins controlling apoptosis directly or 
indirectly have been incorporated into the analysis. The data reviewed here 
provide a mechanistic link between the apoptosis alterations and development of 
radiation-related cancer in the 30-year post-Chornobyl period. We suggest that 
the type of mutations arising from misrepair of DNA double strand breaks (gene 
fusion and amplification) is the initial signature event in radiation-induced 
thyroid cancer. Much work has to be done over the next years to elucidate 
central questions related to the nature of human radiation carcinogenesis. This 
article is part of a Special Issue entitled "The Chornobyl Nuclear Accident: 
Thirty Years After".