Molecular epidemiology of childhood thyroid cancer around Chernobyl

Abstract

Fifteen years after the Chernobyl accident, the accumulative data strongly suggest the direct involvement of radiation fallout exposure on human health, especially thyroid tumorigenesis. Based on the clinical data from Chernobyl, the summary of the second Chernobyl Sasakawa project has been introduced first. The comparative study of thyroid diseases demonstrates the likelihood of short-lived radioactive iodine on thyroid cancer in the children born before the Chernobyl accident. Next, at the standpoint of recent molecular analysis of thyroid carcinogenesis, many reports now indicate evidence of a high incidence of ret/PTC gene rearrangement in childhood thyroid cancer tissues. Besides ret/PTC gene rearrangement, the disturbance of the response of intracellular signal transduction to radiation exposure is also important in thyroid cells, and results demonstrate that radiation exposure could cause abnormal thyroid cell proliferation specifically through constitutive activation of intracellular target molecules via membrane lipid breakdown, and subsequently disturb the apoptosis-prone pathway. It is now urgent and to search for radiation-induced signature genes and/or target molecules using the newly established Chernobyl Thyroid Tissue Bank. Therefore, the late effect of radiation, even in the lower dose on the human thyroid glands, should be monitored carefully for the radiation-sensitive vulnerable group for a longer period, especially around Chernobyl.