186 Resistance of Mice to the Growth of Cancer. 



specific hemolytic, cytolytic, and precipitin reactions. As pointed out in 

 Second Scientific Eeport, 1905, pp. 32 — 33, they are of far greater delicacy, 

 and have only been revealed by using living cells as indicators. 



The experiments recorded in this paper give further evidence of the great 

 delicacy and the very narrow range of variations in the soil furnished by 

 the living animal, within which growth can proceed or is inhibited. Growth 

 has only been hindered by the intervention of mouse tumour or normal 

 mouse tissue, to an infinitesimal degree by the normal tissues of the rat, 

 and not at all by those of less nearly-related animals. We therefore feel 

 justified in concluding that these reactions are parallel to those others 

 whereby blood relationship has been established (Uhlenhuth). 



When we attempt to formulate an explanation of the nature and 

 mechanism of the changes leading to inhibition of growth, it must be clearly 

 kept in mind that. the evidence is almost entirely in the direction of showing 

 an alteration in animals whereby they are unsuitable for or inimical to the 

 establishment of grafts. There is no satisfactory evidence of an induced 

 action on growing vascular ised tumours, but only one against newly- 

 introduced grafts. Spontaneous absorption, depending largely on alterations 

 from the side of the parenchyma, is sufficiently frequent to enforce caution 

 in assuming an artificial alteration in the resistance of animals already 

 carrying growing tumours. Complete absorption is necessary to induce 

 absolute refractoriness to subsequent inoculation. Hence the action of 

 various procedures in inhibiting the growth of grafts is not necessarily or 

 even probably due to a direct action on the parenchyma cells. 



The connective tissue reaction, which a cancerous graft elicits, is taken 

 advantage of by the cancer cells and acquires characters specific for each 

 sporadic tumour. It is immaterial whether this reaction is protective on 

 the host's part, and only not effective because the slight differences between 

 the tumour cells and normal mouse tissues* do not sufficiently stimulate the 

 protective process. The necessity which exists on the part of the cancer 

 cells for this reaction if they are to continue to grow, renders it possible that 

 a refractory condition may indeed not have anything to do with an action 

 against the cancer cells, but, on the contrary, be due to an alteration of the 

 connective tissue of the host which hinders it from supplying the necessary 

 connective tissue reaction. The possibility must also be entertained that the 

 alteration is directed against the chemotactic influence which may be pre- 

 sumed to be exerted by the cancer cells on the connective tissue of the host. 

 Our own experiments have not yet given satisfactory direct evidence of an 



* Once the tumour cells are dead they excite an energetic phagocytosis. Cf. figs. 43 — 48, 

 ' Second Scientific Eeport,' Part 2, 1905. 



