302 Drs. Bashford and Russell. Homogeneity of [Jan. 17, 



Investigation lias also been made of the details of the processes at the site 

 of the re-inocnlation iia mice 10 to 12 days after the primary inoculation of 

 tnniour " 199." It has been found that there is an inhibition of the stroma 

 reaction in those mice whose primary tumours had showed a slowing up in 

 their speed of growth, or had begun to diminish in size. A study of the 

 actual mechanism of resistance to re -inoculation points unambiguously to its 

 being due to the induction of an active resistance to the cancer cells 

 identical with that described for normal animals (-1). It is possible i'or 

 a mouse bearing a growing tumour to be actively resistant to re-inoculation, 

 a fact which has already for other reasons been attributed to concomitant 

 immunisation arising from absorption of a portion of the already established 

 timiour (9). The successful re-inoculation of mice bearing the most rapidly 

 growing "199" tumours is easily understandable on this basis, as in this 

 case the amount of absorption of tumour tissue is practically nil, and 

 resistance has not been established. The assumption of a t^pecial " atreptic " 

 immunity in the case of animals already bearing tumours, where the host is 

 passive and the tumour active, by withdrawing food, to explain the failure in 

 certain cases to re-inoculate an animal the bearer of a growing tumour, 

 is superfluous. 



An immunity developing when cancer of one species is inoculated into 

 another species of animal has been assumed by some workers to be an 

 immunity against cancer. Only the most rapidly growing of mouse tumours 

 when inoculated into rats grow for six to eight days according to 

 Ehrlich(lO), quite as well as in mice, but after this date they become 

 absorl)ed, and tlie animals are then actively innnune. If lemoved at the 

 height of their development from the rats and inoculated into mice or rats, 

 Ehrlich states they grow in the former but do not grow in the latter. Tlu^ 

 temporary growth in rats is explained by Ehrlich as another instance of 

 atreptic immunity due to the absence in the rat of an unknown specific 

 substance necessary for the growth of mouse tumours. The transitory 

 growth of mouse tumours in rats has lieeu shown to be common to those of 

 slow growth (4) as well as of rajjid growtli, including Jensen's carcinoma, for 

 which the possibility was denied. In tlu; third scientific report of tlie 

 Imperial Cancer Research Fund, tliii natuni of tlu' tissue reaction was 

 demonstrated when I'ats, inoculated 14 diiys i)r(;vi()usly with mouse tumour, 

 were re-inoculated, i.r., while they were actively innnune iigainst mouse 

 tumours. Eurther, this immunity was shown to be of a dillerent character 

 from the iunnunity of inice against mouse tumours. When rats innnunised 

 with mou.se tumours were inoculated witli "early stag(!s " of a mouse 

 tumour, tlu^re took j)lace an active destruction oi' the introduced tumour 



