IMMUNITY IN TUMOR TRANSPLANTATION 403 



an active immunity which had not been demonstrated previously may become 

 manifest, but there is reason for assuming that it was actually present already 

 while the tumor was growing in the host; (3) after regression of a homoiog- 

 enous or heterogenous tumor, when an animal as a rule is found to be 

 immune to a second inoculation of the same or of a similar kind of tumor; 

 (4) after inoculation of normal tissues or of pieces of tumor unable to give 

 rise to the formation of tumors ; to a certain extent, animals thus treated are 

 immune to the growth of a piece of tumor subsequently inoculated. We shall 

 now describe the essential characteristics of each of these types of active 

 acquired immunity, and shall also discuss (5) the presence of immune sub- 

 stances in the bodyfluids or tissue extracts of an animal which has acquired 

 an active immunity against a tumor, as well as (6) the significance for im- 

 munity of cellular reactions in the host against tumor transplants and lastly 

 (7) the presence in tumor cells of antigens other than organismal differ- 

 entials. 



(1) Concomitant immunity. From a theoretical point of view, this is per- 

 haps the most important and most generally occurring type of active acquired 

 immunity. It can be tested by inoculating animals, which already are the 

 bearers of such transplanted tumors, a second time with tumor pieces and 

 comparing the number of takes and the' growth energy of the second tumors 

 with those of the first. This immunity is elicited only if the organismal differ- 

 entials of host and transplant differ, and is demonstrated the more readily, 

 the greater the difference between the organismal differentials. It is very 

 marked when a tumor grows for some time in a heterogenous host ; homoiog- 

 enous tumors also give rise to immunity, but the growth of an autogenous 

 tumor graft does not have this effect, nor is it observed if a spontaneous tumor 

 is propagated through transplantation in the same closely inbred, homozygous 

 strain in which it originated. 



As we have seen in a preceding chapter, the experiments of Fleisher and 

 the writer, as well as those of Haaland, prove that the growth of an autogenous 

 spontaneous tumor does not influence the subsequent development of a 

 homoiogenous inoculated tumor; conversely, the growth of a homoiogenous 

 tumor does not affect the growth of autogenous tumor transplants and of 

 metastases from the autogenous tumor. 



However, in addition to differences in organismal differentials between 

 host and transplant, other factors may enter into the production of con- 

 comitant immunity. This is clear if we compare the varying conditions under 

 which this type of immunity has been observed. Strieker noted that at a cer- 

 tain period in the growth of a homoiogenous lymphosarcoma in a dog, im- 

 munity against a second inoculation developed, and Ehrlich found that the 

 growth of a rapidly growing tumor inhibited the growth of a tumor of the 

 same kind subsequently inoculated. According to Ehrlich and Schoene, the 

 extirpation of the first tumor suspends this immunity and makes possible an 

 inoculation with a second tumor. Ehrlich held that the first actively growing 

 tumor used for its own growth all available growth-substances specifically 

 required for the multiplication of tumor cells, and thus prevented the growth 

 of a second tumor (athreptic immunity). That this interpretation does not 



