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Synergistic Action of Leukemogenic Agents^*

( Department of Anatomy, College of Medicine, University of Illinois, Chicago, Ill., and Departments of Anatomy and Radiology, University of Minnesota Medical School, Minneapolis, Minn.)

1. Although susceptible to the leukemogenic action of x-rays or estrogenic hormone, BALB and CBA mice were relatively refractory to methylcholanthrene. X-rays and estrogenic hormone acted synergistically in accelerating the onset of induced leukemia. Methylcholanthrene did not act synergistically with either x-rays or estrogenic hormone in these strains.

2. In DBA mice lymphosarcoma and leukemia were induced by either methylcholanthrene or x-rays. Estrogenic hormone enhanced the leukemia-inciting potency of either the carcinogenic hydrocarbon or the ionizing radiations, although independent leukemogenic activity of estrogenic hormone in the dose used was not demonstrable in DBA's.

3. Genetic factors determine susceptibility to specific leukemogens acting either independently or in conjunction with others.

4. "Synergism," as used here, denotes increasing, by the simultaneous administration of leukemogens in relatively low doses, the incidence of lymphomas in the first 300–400 days of life beyond the sum of the incidences obtained by the independent action of the leukemogens.

5. The thymus was the most important locus for the synergistic effects of leukemogens (x-rays, methylcholanthrene, estrogen) in accelerating the onset of induced leukemia.

6. In BALB mice radiation restricted to the thymus accelerated the onset of thymic lymphosarcoma when given in conjunction with estrogen, whereas in CBA's thymic radiation was ineffective under the same conditions.

7. Thymic lymphosarcomas developed precociously in BALB mice after the whole body, except the thymus, was subjected to radiation and to relatively small doses (from the standpoint of leukemogenesis) of estrogenic hormone. Since thymectomy abolishes the leukemogenic activity of these agents in BALB mice, it is probable that the radiation effects on the thymus were secondary, or humoral, and were elicited by the action of estrogenic hormone.

^* This investigation was supported by a grant from the National Cancer Institute, National Institutes of Health, Public Health Service.

Received 10/24/52.