350 THE BIOLOGICAL BASIS OF INDIVIDUALITY 



usual active way without undergoing regression. This conclusion is also con- 

 firmed by the fact that regression of a Walker rat carcinoma or a Jensen rat 

 sarcoma did not cause immunity against the growth of the Ehrlich-Putnoky 

 tumor. If the carcinomatous cells had assumed, at least partly, the species 

 differential of the rat, the immunity against the growth of a rat tumor caused 

 by the previous retrogression of a rat tumor in rats should have affected also 

 the Putnoky tumor. On the other hand, the growth of the Ehrlich-Putnoky 

 rat-strain tumor in rats can be prevented by previous inoculation of mouse 

 embryo-skin into the rats. This again indicates that the tumor cells still pos- 

 sessed the species differential of the mouse. If inoculation of mouse embryo- 

 skin induces only a slight retardation of the growth of the Ehrlich-Putnoky 

 tumor in the mouse, this is presumably due to the very strong growth mo- 

 mentum which this tumor possesses in mice. In a similar way, Purdy found 

 in heterotransplantation of fowl tumors into ducks, ducks were made immune 

 to the fowl tumors by a previous implantation of chick embryo, but not of 

 duck embryo. 



However, there is one observation which might suggest that an actual 

 change in the species differential of the Ehrlich-Putnoky tumor growing in 

 rats has taken place. After regression of such a rat-propagated tumor in rats, 

 the latter have acquired an active immunity against the growth of subsequently 

 inoculated Walker and Jensen rat tumors ; rat-propagated Putnoky tumors 

 are more effective in this respect than are Ehrlich mouse-strain carcinomas. 

 But this difference may perhaps be due to the fact that the Ehrlich-Putnoky 

 rat-strain tumors grow much more vigorously in rats than do mouse-strain 

 tumors ; they may therefore be expected to induce a higher degree of im- 

 munity. While there is no reason for assuming that the genetic constitution 

 of the mouse carcinoma cells has been transformed into the genetic constitu- 

 tion of the rat, or that the better growth of these cells in the rat was made pos- 

 sible through a gene mutation or chromosomal change in these somatic cells, 

 still it is possible that certain adaptive changes have gradually taken place in 

 the Ehrlich-Putnoky tumors, which make them more able to overcome the 

 injurious conditions existing in the rat after long-continued propagation in 

 this strange species. Also, in other series of heterotransplantations, adaptive 

 changes of this kind seem to have occurred. These may consist in a gradually 

 increasing growth energy of the tumors in the rat, or in an increasing resist- 

 ance to the injurious rat substances, perhaps caused by a more active absorp- 

 tion and neutralization of such substances by the growing tumor cells. That 

 such an adaptation may take place after heterotransplantation is indicated, 

 also, by the fact that at first the temporary growth of the Ehrlich-Putnoky 

 mouse tumor was accomplished only in very young rats, in which the reac- 

 tion against strange differentials is less marked than in adult animals, and 

 that only in the course of continued transplantations in the rat did the tumor 

 begin to grow well, at least for some time, also in young adult rats. In addi- 

 tion to these adaptive changes, it is conceivable that in the course of continued 

 re-transplantations into rats those metabolic cell activities which lead to the 

 production of the organismal differential, and which in the last analysis 



