抄録
We have proposed a hypothesis that excess risk of ALL following radiation exposure is not caused by induction of ALL-specific translocations but radiation affected on a small number of individuals who already had clonally expanded ALL-specific translocations spontaneously. In the present study, we show that the translocations probably occur in early fetal life. We used epidemiologic data of Oxford Survey of Childhood Cancer (OSCC) by Stewart et al, which showed that diagnostic X ray exposure (about 1 cGy) caused 50% increase of the background risk of childhood leukemia. The logic that we used is; if an early stage has not yet developed ALL-specific translocations, the excess risk should be substantially lower compared with the risk at later stages. The OSCC data showed that trimester 2 and 3 fetuses had the relative risks (RR) of 1.29 and 1.30, respectively, which means that there is no difference in the RR. In fetuses exposed at trimester 1, the RR was larger than 3 while the larger risk cannot be taken at face value because radiation dose per X-ray film was larger and the mean number of films taken was also larger in trimester 1 fetuses. Nonetheless, the trimester 1 fetuses do not seem less sensitive to radiation exposure. We conclude therefore that the ALL-specific translocations are most likely produced in the first trimester.
