Ill VIRUSES AND CANCER 855 



acceleration of onset of leukemia in AKR mice by the inoculation of cell-free filtrates 

 of brain tissue extracts derived from leukemic mouse and human brains. 



Maternal resistance factor. MacDowell and Taylor (1948) reported the presence 

 of a "maternal resistance factor" in StoLi mice. If high leukemia C58 mice were 

 foster-nursed by StoLi females the appearance of leukemia was delayed. Law ( 1 954) 

 confirmed MacDowell's work on the maternal resistance factor. 



\n reciprocal Fi hybrids between the high leukemia C58 and several low- 

 leukemia strains, leukemia appears later if the mothers are of the low rather than 

 the high-leukemia strain. The incidence of leukemia is lower and the age of onset 

 later in the offspring of older (as compared with younger less than 32 weeks) 

 mothers (MacDowell, 1955; Liebelt, A.G., 1957). Such differences in leukemia 

 incidence are demonstrated best in females (Liebelt, A.G.. 1957); androgenic 

 hormone may delay leukemogenesis to such a degree that the influence of maternal 

 age is not detected in males. In all Fi hybrid mice between high- and low- 

 leukemia strains, leukemia appears very much later than in the high-leukemia 

 stock. Life expectance of Fi hybrids is comparably greater. 



Is the "maternal resistance factor" of MacDowell actually indicative of a low 

 level of leukemia-inciting agent in female mice? With transfer oHess agent it might 

 appear that a positive resistance factor has been transmitted. Foster-nursing ex- 

 periments have in the past employed low-leukemia nurses for high-leukemia 

 newborn mice (Kirschbaum and Strong, 1942). High-leukemia nurses might pro- 

 vide "agent" to accelerate the development and increase the incidence of leukemia 

 in low-leukemia strains; the investigations of Schwartz et al. (1957) are of interest 

 in this regard. 



{d) Parotid and skin tumors of the mouse 



Neoplasms (carcinomas) of the parotid gland have appeared in C3H and AKR 

 mice injected with leukemia extracts (Gross, 1955, Stewart, 1955). Such tumors 

 have occurred spontaneously in one line of C3H mice (Law et al., 1955), and in 

 C58 mice injected with cortisone (WooUey, 1954). But they do not occur in certain 

 inbred stocks (Dulaney, 1956) unless the newborn is injected with mouse tissue 

 extracts. In the experiments of Gross (1955), only infrequently did mice develop 

 both parotid tumors and leukemia. It is his conclusion that a different virus is 

 involved in each of these diseases. 



Fibrosarcomas have developed at the site of inoculation of mouse tissue extracts 

 (Gross, 1955). It was assumed that these do not occur spontaneously in C3H mice, 

 the recipient strain. Dunn et al. (1956) have reported the occurrence of similar 

 tumors in aged C3H mice. 



{e) Mature of the tumor viruses 



The accumulated evidence suggests that the mouse tumor viruses may accelerate 

 the onset of diseases which occur spontaneously (leukemia, mammary cancer, 

 parotid carcinoma, fibrosarcoma of skin). Filterable factors derived from these 

 neoplasms have caused the early appearance of these neoplasms in hosts which 

 develop them later in life "spontaneously". In the case of leukemia the agent must 



Literature p. 8yo 



