IMMUNOGENETICS OF TUMOURS IN CHIMERAS 169 



larity in the effects of cortisone and X-rays on the lymphatic 

 system and the immune mechanism, one is tempted to speculate 

 further on the possible role of resistance to metastasis in con- 

 trolling its development. There is obviously no direct indication 

 that an immunological-hke mechanism participates in controlling 

 the formation of metastasis of the primary tumour, or of isologous 

 grafts. It is, however, of interest to note that chemically induced 

 tumours (which usually do not form metastasis) have recently been 

 shown to ehcit a specific immune response in primary or isologous 

 hosts. Such specific antigenicity was found both in tumours 

 produced by methylcholanthrene (Prehn and Main, 1957; Klein 

 et ah, i960) and by benzpyrene (Feldman and Globerson, un- 

 published). Whether the immune response ehcited by such 

 tumours in isologous systems is associated with the suppression of 

 metastasis, remains a subject for further experimental tests. 



The formation of metastasis by tumours which metastasize via 

 the blood circulation, may involve a different mechanism. Zeid- 

 man (1961), in studying the effect of cortisone on lung metastasis 

 of the Brown Pearce carcinoma injected intravenously as a cell 

 suspension in rabbits, claims that in this case cortisone increased 

 the incidence of capillary arrest of tumour cells. 



Ittimunogenetic changes in tumour cell populations 



In contrast to the results obtained by rejection of homografts 

 of two strain-specific tumours by genetically foreign spleen cell 

 chimeras, which are presented in Table I, transplantation of a third 

 tumour, the sarcoma SBLi, gave different results: here, even 

 transplants on foreign spleen chimeras (C3H->C3H) gave 

 successful homografts. Lethal takes were obtained both in 

 foetal-treated and in spleen-treated C3H hosts. The progressive 

 growth of the SBLi in immunologically reactive chimeras could 

 be attributed either to a low susceptibility of the tumour to the 

 immune response formed in the C3H chimera, or to changes 



