338 H. B. ANDERVONT 



distinction between such efforts, this presentation is divided into three parts, 

 namely, host-virus relationships as they concern; (1) the role of the virus in 

 producing tumors; (2) the latency of the virus; (3) the age factor in response 

 to the virus. 



1. The Role of the Virus 



The production of any virus tumor is the result of interactions between the 

 host, the virus, and the environment; breast cancer in mice is no exception. 

 Discovery of the virus added another such influence to those of heredity and 

 hormonal stimulation. Genetic factors control the degree of susceptibility of 

 mammary tissues to the virus as well as the ability of the mouse to propagate 

 the virus. They also control the susceptibility of mammary tissue to hormonal 

 stimulation and may modify the hormonal stimulation of the host. Hormones 

 exert a pronounced influence through their control of the development of 

 mammary glands and thereby provide a substrate for the action of the virus; 

 mammary tumors do not appear in mice in the absence of estrogenic stimula- 

 tion. 



All three factors, genetic, hormonal, and viral, are known to be important 

 and it is the consensus that a tumor can be produced when a deficiency in one 

 factor is compensated by an increase in one or both of the other factors. 

 Other influences, such as diet and overcrowding (Andervont, 1944), are known 

 to affect the occurrence of the tumors. This attitude is a natural outgrowth 

 from previous acceptance of the importance of hereditary and hormonal 

 influences in the appearance of the tumor before the virus was exposed. The 

 important point is that, with this virus-induced tumor, the virus from the 

 first has not been the sole object of attention; instead, it is considered as part 

 of a complex interplay of forces leading to the production of cancer. And this 

 is important because, with the acceptance of the virus as but one factor in the 

 cancer process, the virologist enlarges his viewpoint of the viral etiology of 

 cancer. The virus of mammary cancer in mice was not discovered by viro- 

 logists, but by geneticists who were interested primarily in an evaluation of 

 the genetic factors concerned with the occurrence of the tumor. 



In recent years, even the necessity of the virus has been seriously questioned, 

 and, to date, most evidence supports the idea that mammary tumors can 

 arise in mice in its absence. In an early review, it was pointed out (Andervont, 

 1945a) that mammary tumors occurred in a few hybrids derived by mating 

 low-tumor strain females to high-tumor strain males, but the incidence of 

 such tumors was very low. An opportunity to investigate the problem 

 presented itself when it was found that first generation hybrids born to low- 

 tumor strain BALB/c females and high-tumor strain C3H males showed a 

 high incidence of mammary tumors (Andervont, 1945b). These tumors were 



