146 



V. DRASIL 



the mice die after a shorter period. It is rather surprising in this case that 

 the influence of radiation can be demonstrated even on mice irradiated thirty 

 days prior to being injected with EAT. 



For the time being, only hypotheses may be expressed about the mech- 

 anism of the influence of irradiation described above. In the first place we 

 might consider the reduction of the immunity reaction as a result of irradia- 

 tion. However, from the work of Ilbery (Ilbery et al., 1958) and those of other 

 authors dealing with immunity reactions against tumour cells after irradiation 



Days 

 35 



30 



25 



20 



15 



101 

 5 



1 1 day [ after 



n 30 days ) irradiation 



20r 60r I80r 20r 60r I80r 

 ^ ' ^ . ' 



n 



Fig. 1. 



it follows that the ability to form antibodies reverts to normal one month 

 following irradiation even after doses of radiation higher than 200 r. This 

 must occur more quickly after doses of 180 r, 60 r or 20 r. Consequently, we 

 presume that the suppression of the immunological activity will not be the 

 reason why irradiated mice die faster after being injected with EAT. 



When "metastases" are formed after an intravenous injection of EAT, the 

 state of the capillary vessels, in which the cells are intercepted and the walls 

 of which they destroy in the course of their further growth, most probably also 

 plays an important role. It is likely that irradiation may result in some damage 

 in the wall of the capillaries, or that it may produce in the adjoining connec- 

 tive tissue some changes that promote the formation of the tumour, and its 

 further growth, 



REFERENCE 



Ilbery, P. L. T., Koller, P. C, and Loutit, J. F. (1958). J. nat. Cancer Inst. 20 

 1051. 



