Myeloid leukemia, one of the earliest recognized examples of radiogenic cancer (see Furth and Lorenz, 1954), is conspicuously increased in frequency among people surviving high-level, whole-body ionizing irradiation (Brill et al., 1962; Wald et al., 1962). Because of t,he importance of this neoplasm as a radiation hazard, the mechanisms and kinetics of its induction merit systematic investigation. For this purpose, mice of the R F strain are ideally suited, since a large proportion of them develop myeloid leukemia in response to relatively small amounts of whole-body radiation. Observations on the radiologic and host factors influencing the development of the disease in such animals are surveyed in this article.Clinicopathologic features. The myeloid leukemia encountered in irradiated R F mice is indistinguishable from that occurring spontaneously in mice of this and other strains. Clinical, hematologic, and pathologic features have been described elsewhere (see Dunn, 1954;Upton and Furth, 1954; Parsons et aE., 1962). It is noteworthy, however, that the disease closely resembles chronic granulocytic leukemia of man. The leukocytes in the peripheral blood characteristically show a high degree of maturation, and the infiltrations in the marrow, spleen, and liver are exclusively of granulocytes and their precursors. A predominance of myelocytes and more primitive forms is seen only after serial transplantation of the neoplasm. Whether the clinical course of the primary disease is acute or chronic cannot be determined from the information at hand, since its diagnosis has been made ank rnortem only in terminally ill or moribund mice.Incidence in relation to radiation dose. Apart from the influence of host factors, which is mentioned below, the incidence of leukemia at any given dose level varies with the dose rate; the number and frequency of exposures; the linear energy transfer (LET) of the radiation; and the fraction of the body irradiated.When the mice are exposed to whole-body X or y irradiation in a single, brief exposure ($100 rads/min.) early in adult life (five to ten weeks of age), one finds that the incidence is increased several times above normal by a dose of 100 r, reaches maximal levels at 200-400 r, and declines at higher dose levels, the peak response in males (FIGURE la) exceeding that *Operated by Union Carbide Corporation for the United States Atomic Energy Commission. 189