Olive Gates

The Induction of Leukemia and Life Shortening in Mice by Continuous Low-Level External Gamma Radiation

Continuous external gamma radiation throughout life at the rate of 0.062 rad/day failed to induce leukemia in A/Jax mice, but did in 55% of RAP mice. Sixty percent were lymphatic, 23% myelogenous, and 17% of other types of leukemia. In RAP mice there was no significant shift in frequency of leukemia in each of five successive generations. The experimental mice were compared with mice irradiated from an internal radiation source and also controls. The incidence of leukemia in control mice was 7%. The high incidence of leukemia in this irradiated population cannot be explained, but the probability is strong that the population evolved from highly leukemia-susceptible mice.

Leukemia and lymphoma in irradiated parabiont rats.

Leukemia and lymphoid tumors each have a 2% spontaneous rate in NEDH rats. Rats are less prone to such tumors than mice. Parabiosis of syngeneic rats permits one partner to survive a whole-body X-ray exposure of 1000 R if the other partner is shielded. Parabiosis alone induced a slight increase in the rates of incidence of both leukemia and solid lymphoid tumors, to about 5%. Exposure of one parabiont partner to 1000 R did not increase the incidence rates of these tumors significantly in either partner and sharply decreased the incidence rate of lymphosarcoma in female pairs. Monocytoid and myeloid leukemias were the more common types. Leukemia was often but not always shared by both partners of a pair. The solid lymphoid tumors tended to respond similarly following parabiosis and radiation. These tumors were usually restricted to one partner. Their incidence rates did not differ significantly between the irradiated and shielded partners, for lymphosarcoma 0.3% in the irradiated and 1.0% in the shielded a...

Mammary tumorigenesis through irradiation of mice

RAP mice, possibly harboring mammary tumor virus (MTV), of representative ages were exposed to limited or lifetime whole-body continuous gamma and to fractionated x-irradiation. Doses varied from 30-2100 R and dose rates from 0.062-121 R/day in the two series GA and PN in which mammary cancer incidence was elevated. Induction of mammary cancer was found to be related to the dose range for ovarian tumorigenesis, 30-500 R, but unrelated to age when exposed. There was no statistically significant correlation between mammary cancer and ovarian tumors. Active MTV infection was suggested by cancer-prone litters in one irradiated (PN U + SR) and one unirradiated series (OCB). Unirradiated descendents of perinatally irradiated mice with an inherited hormonal disorder had a lower incidence of mammary cancer than stock virgin mice. The balance of evidence pointed to induction of mammary cancer through systemic change set in motion by irradiation.

Spontaneous and radiation-induced benign tumors in parabiont rats.

Spontaneous benign tumors are present in nearly half of NEDH rats. A single whole-body exposure of 1000 R X radiation delivered to a rat supported by a shielded parabiont partner induced high incidence rates of benign tumors in several radioresponsive organs: ovary, 49.7%; adrenal medulla (males, 23.9%; females, 15.2%); mammary tissue (females, 19.6%); islands of Langerhans (males, 15.3%); and liver (cholangiomas) (males, 7.4%; females, 13.8%). Both hormonal imbalance and radiation effects appear to be involved. Parabiosis decreased the incidence of pheochromocytoma, but irradiation of a partner increased it. Mammary tumors occurred on the average 200 days earlier in irradiated rats than in their unirradiated controls. Benign tumors rarely affected health. The incidence was not increased in most organs following irradiation. Three control series were used: single rats, control parabiont rats and the shielded partners of the irradiated partners. Although endometrial polyps were more frequent in irradiated than in shielded partners, they probably resulted from hormonal imbalance. Adenomas of the pituitary were most frequent in shielded female parabiont partners (16.0%). Their incidence was decreased by radiation to 4.2%. Most types of benign tumors rarely progress to malignancy.

Incidences of types of cancer in irradiated parabiont rats.

A total-body dose of 1000 R X radiation to 1252 male and 1366 female NEDH rats protected by permanent parabiosis to an untreated partner yielded respective cancer incidences of 42.7 and 38.3% within mean life-spans slightly less than single controls. These incidences were significant at the 1% level of probability compared with lower rates in shielded partners as well as in over 600 control parabiont partners and 700 single controls in which both sexes were nearly equally represented. Significant cancer incidences were induced in skin and islet cells of males, soft supporting tissue, renal tubules, bone of males and females, and ovary. Parabiosis per se provided local conditions conducive to the development of sarcomas, possibly enhanced by radiation, in anastomosed tissue as well as systemic changes promoting the spontaneous development of lymphoma and leukemia in females and inhibiting that of mammary carcinoma in females and malignant pheochromocytoma in males. The effects in females were largely cance...