Studies on Radiation-Induced Mammary Gland Neoplasia in the Rat: V. Induction by Localized Irradiation

Abstract

Previous studies from this laboratory had demonstrated that a single large whole-body x-nay exposure of SpragueDawley rats was followed in months by a large increase in the incidence of maximary gland neoplasia. In addition, the dose-effect relstionship appeared to be linear within limits, and intact ovarian function was demonstrated to be necessary for maximum incidence of neoplasia. In the present dose-effect relationship appeared to be linear within limits, and intact ovaria function was demonstrated to be necessary for maximum incidence of neoplasia. In the present experiments, designad to determine if the breast tissue must be directiy irradinted for maximal neoplasia indnction, groups of approximately 30 female Sprague-Dawley rats were irradiated on the fifty-fifth day of age as follows: 400 r total-body irradiation; 400 r entire left half of body; 400 r to chest; 400 r to lower half of body; 400 r with one hind linhb shielded; and 400 r through a gnid. With half-body exposure and with exposure through the gnid, approximately one-half of the total number of neoplasms seen after totalbody irradiation was observed. Shielding of the leg had no effect on the incidence of neoplasia. With half-body irradiation, more than 90% of all breast neoplasms occurred inmore » tissues exposed directly to the beam. The results indicate cleanly teat direct radiation injury to the breast is necessary for an increased incidence of radiation-induced neoplasia under the conditions employed. It appears from these and previous studies that radiation-indnced "primary" damage in the target organ is necessary for an increased incidence of the neoplasia observed, but that the primary damage may lie dominant and not manifest itself maximally as neoplasia unless an additional secondary mechanism (presumably cyclic ovarian activity in the data presented) is operative, The implications of the results with regard to a possible somatic mutation mechanism of radistion neoplasia induction are discussed. (auth)« less