less than the carciastenic response In the att ae This argument would eppcar to have merit since mitotic dcath of cells, of well as recucing the general viability of the tissue, would also reduce the number of irradiated oh. m canceptualization of all rediction errcirogornesis as a sing w Urually ianlicit in this argument isa oa Oo a — rolls with carcinogenic potential. . Lynn wPEC a . injury process. To confirm this argument, there is a respectable literature in which carcinocenesis is described és occurring after doses of radiation that are sufficiently local es to not be organism lethal, and that are sutticieently high for che 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 ‘. ' Tistic cemm2tence is qrevter than 7% is small conpared with the cancer induction in the regime where mitotic compatence is much Tess than There are several points to be made here. lis. ef Loss of mitotic competence and carcinogenesis are two indices of radiation effect in tissue. They cannot be independent, and their relationship can tell us something about some radiation carcinogenesis. Mitotic comnetence is nct gensrally related in a linear way to carcinogenic response.’ loreover, it As a major anomaly that an increased carcinogenic response is observed in cose 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. Hitotic cemmatence of a cell population decreases exponentially with Tnereas ing aipha-radiation dose and is a fairly qenaral indoz of radiation effect in tissue. $ RT oy SPE ¥, Bae es an Poet? , WH radiation carcinogenasis universally ETNCRT A a Ht ‘gysepehs OB free ior, yg abryas ut ay th. Bitiu ES Me aR tt Ay re re sa OR 7 oy wee whe,