Cr Ce ” ay ¢ . “ ? "oe less than the carcinazenic response in tha latter. This argument would appear to have merit since mitotic death of cells, cf well as reducing the soneral viability of the tissue, would also reduce the number of irradiated cells with carcinogenic potential. Usually implicit in this argument is a conceptualization of all radiation carcinogenesis as a single-cell, direc.injury process. To confirm this argument, there is a respectable literature in which carcinogenesis is described as occurring after doses of radiation that are sufficiently local as to not be organism lethal, and that are sufficiently high for the fraction of mitotically competent cells to be greatly reduced, i.e., to 1% or less. Unfortunately, in at least some of these experiments, carcinogenesis is inversely related to the fraction of mitotically competent cells, i.e., cancer induction in the regime where _mitotic competence is greater than 1% is smal] compared with the cancer induction in the regime where mitotic competence is much less than 1%. There are several points to be made here. Loss of mitotic competence and carcinsgenesis are two indices of radiation effect in tissue. They cannot be indeperdent, and their relationship can tell us something about some radiation carcinogenesis. Mitotic competence is not generally related in a linear wey to carcinogenic response. Moreover, it is a major anomaly that an increased carcinogenic response is observed in dose regimes associated with greatly reduced mitotic competence: It is difficult to reconcile this result with any single-cell, direct-effect origin for radiation induced cancer. Mitotic comnetence of a cell population decreases exponentially with increasing alpha-radiation dose and is‘a fairly ganeral index of radiation effect in tissue. If radiation carcinogenasis universally