Abstract
The mechanism of radiation-induced leukemia has been supposed to be direct effects that may be quite different from that of solid cancers, because of a shorter latent period and higher relative risk in leukemia than in solid cancers. Nakamura (2003) proposed the hypothesis that radiation exposure does not initiate a normal cell but accelerates the clonal expansion of the chromosomal translocation that arises predominantly in utero. We focus on the age pattern of ALL and AML in the A-bomb survivors. If radiation exposure acts only as a initiating event, a rapid increase in leukemia in several years after exposure is not available by the two-stage stochastic model that involves clonal expansion of the chromosomal translocation such as TEL/AML1 which probably leads to ALL., Since the frequency of excess ALL in adults at exposure is lower than in children at the same dose, the dose would contribute to a smaller influence on cell kinetics in adults than in children.
