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



agreement. These difficulties are associated more especially with the results 

 following upon the secondary inoculation of animals already bearing tumours 

 as the result of primary inoculation. Some authors liave succeeded where 

 others have failed to obtain secondary tumours in this way. The methods 

 by which secondary inoculations can be successfully carried out, the import- 

 ance of dosage,* and other technical details, have been fully explained in a 

 series of papers, and the contradictory results harmonised (3, 4, 5). It is, 

 however, necessary to meet hypothetical explanations of the reasons why a 

 secondary inoculation may fail, by recording the results of actual observation 

 of the processes responsible and comparing them with those following the 

 induction of active resistance in normal animals. Therefore, the histological 

 details of the process have been ascertained by examining the site of 

 re-inoculation at definite intervals. This method is conveniently called the 

 examination of "early stages."f By its means the true nature of the trans- 

 plantation of cancer was demonstrated (6, 7), and later it revealed how important 

 for the implanted cancer-cells was the provision of a specific supporting and 

 nutritive scaffolding by the tissues of the, new host (8). It also demonstrated, 

 that in mice rendered resistant to carcinoniata, there was a failure to supply 

 this specific scaffolding, and hence the conclusion was arrived at that 

 actively resistant animals robbed the cancer-cells of the chemiotactic powers 

 they exercise on the connective tissues of the host (4). This failure of 

 the specific stroma reaction was seen both when resistance was induced 

 by the previous absorption of tumour tissue, and l)y the previous absorption 

 of normal tissue — whether adult or embryonic — of the same species. For 

 the elucidation of the mechanism of resistance there is, at present, no 

 alternative to actual observation of the site of the inoculation of cancer-cells 

 in livhig animals. Without resort to tliis laborious method the hypothetical 

 assum])tion of an atreptic imnuniity was advanced io explain why a 

 secondary inoculation may fail in an animal already bearing a tumour. l>y 

 em])loying it the facts recorded in this paper have been elicited ; they 

 harmonise with wliiit has been stated elsewhere on the successful re-inoculation 

 of animals ali'eady Ijeariiig tumours, and show that the resistance which may 

 exist to re-inoculation uiidci- these circumstances is identical in its nature 

 and mechanism with that which can be induced in normal animals, i.e., in 

 t!i(! absence of a tuiiioui'. 



Jt is immaterial whicli of the 65 tumour-strains growing in the laboratory 



* It i'h irii|)0H8il)le to comparo the rate of growth of the tumour.s following inoculation 

 if t li(! amount of material inoculated as the starting point of growth is not stated. This 

 factor Mtill continues to he neghictcul, ev(;n in the most recent investigations of tinnour 

 growth. Cf. Moi'cschi, ' Zeitschrift f. Iniiniinitiitsfoisclinng,' !!)()!). 



+ l^'ull}' (IcscrilK'd in the Sciciitilic KciHu ts of tlif lnii)ori;(l (Jancer Research Fund. 



