1910.] ]i'c.<iifftance to Implantation of Mrdic/nant New Growthsf. 299 



plantations performed on tlie same date, and that transplantation can be 

 sueciOssfuUy performed in animals in which tumours have already developed 

 14 days to 10 weeks after the first effective transplantation, i.e., both when the 

 primary tumour is small and when it has attained a large size." These 

 positive results appeared to be important, first, because of their correspondence 

 with the dissemination and formation of metastases in the normal course of 

 tlie progress of cancer in man, and, secondly, because they afforded a basis for 

 studying the conditions, favourable and unfavourable, to the establishment of 

 secondary implantations in animals already bearing tumours, and hence had 

 also an indirect bearing on the control of natural metastases. Therefore, 

 these observations formed one of the starting points of our studies on the 

 induction of resistance to the inoculation and growth of cancer. Their 

 importance was eidianced later by the success attending efforts to reproduce 

 experimentally both the local infiltrative and the disseminated lesions of the 

 disease. 



Other investigators, who, at a later date, were not so successful, either in 

 re-inoculating animals already bearing tumours, or in reproducing tlie 

 lesions of dissemination, have quite naturally drawn conclusions opposed to 

 those drawn by us; for example, in April, 1906, Ehrlich reported "If 

 metastasis formation be imitated experimentally by re-inoculating animals 

 8 to 10 days after they had been successfully inoculated with a rapidly 

 growing tumour, then the second inoculation, whether it be made with the 

 same or with a different tumour, does not take with few exceptions " (1). 

 Ehrlich was led to attach enhanced importance to his observations by the fact 

 that metastases were rare, or, if present, only of microscopical size, in his 

 inoculated animals. He sought an explanation common to tjhe two groups of 

 observations in the assumption of " atreptic " immunity, meaning thereby 

 that the rapidly growing tumour prevented successful re-inoculation and the 

 establishment of metastases by withdrawing special nutritive substances 

 (Sidjstance X) from the circulation. The idea of "atreptic" immunity has 

 been extended to explain also the transitory growth of mouse tumours in rats 

 by assuming that growth ceased when the hypothetical Substance X, intro- 

 duced with the graft, was exhausted. Ehrlich (2) modified his standpoint in 

 1908 in so far as to admit that re-inoculation may be successful although he 

 maintains that the secondary tumours remain smaller than the corresponding 

 tumours in control animals, and therefore he adheres to his assumption of the 

 existence of an " atreptic " immunity. 



The foregoing summary shows that the elucidation of the nature of active 

 resistance to cancer has been complicated both by contradictory observations 

 and by conflicting explanations of facts, regarding which there is complete 



