Radiation as a Carcinogenic Agent

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Abstract
An examination of current knowledge concerning the mechanism of radiation carcinogenesis was made from the standpoint of its possible bearing on human carcinogenesis at low levels of radiation. In a few cases, notably lymphomas and ovarian tumors in mice, it is obvious that the response is indirect and works through a physiological mechanism involving more than the irradiated cell. These instances show the greatest variation between species. Although local irradiation yields tumors in the directly irradiated area, an indirect mechanism is also apparent, in that there is a considerable latent period during which successive tissue changes take place leading eventually to autonomous tumor growth. The latent period is probably related to the life span of a given species. Present evidence indicates that intense local irradiation is somewhat wasteful of the energy involved, with respect to cancer production. This has not been satisfactorily tested at low dosage levels. A single irradiation can be effective, but good evidence as to the effect of divided doses is lacking. The influence of ion density and dose-response relationships, although partly understood, require further investigation. Some difficulties with the somatic mutation theory have been discussed. Although a cellular mutation may be one necessary step in tumor formation after irradiation, the present evidence suggests that it must play a subordinate role.