544 



RADIATION lUOLOGY 



dcvolopincnt time and tluit the idt'u tluit ultruviolcl radiation acts by 

 forming tumor cells which immediatolj' adopt a new and thenceforward 

 constant rate of growth is not consistent with the experimental hndings.'-' 

 While this may not constitute an absolute negation of the idea of somatic 

 mutation, it is evident that the hypothesis must be radically' modified if it 

 is to lit the experimental data. It may be seen that these cjuantitatixc 

 experiments on the induction of cancer by ultraviolet radiation pose 

 serious difficulties to theories of carcinogenesis which have been quite 

 widely accepted by various groups of work(M-s. 



Another tentative theory will now be descril^ed, which is treated else- 

 where in more detail than can l)e afforded in this chapter (l^lum, 1950b). 

 The theory is a quantitatively descriptive one whi(;h does not attempt 







3 

 o 

 q: 

 O 



UJ 



> 

 I- 

 < 

 _] 

 tij 

 q: 



TIME [i) 



Fig. 14-5. Diagram to illustrate progrossivo accolcratioii of relative growth rates. 



thus far to postulate any intimate mechanism for carcinogenesis, but 

 suggests a frame wdthin which such a mechanism needs to be fitted. 



The theory is based on the postulate that successive doses of radiation 

 progressively accelerate the relative rate of cell proliferation, each dose 

 bringing about an increase in rate. In formulating an approximate model 

 to describe this progressive acceleration of growth rate, \ve begin by 

 rewriting Eq. (14-2): 



^ = G- (14-9) 



The left-hand member of this ecjuation represents the relative instan- 

 taneous growth rate, which can be plotted against time, as in Fig. 14-5. 

 If the rate remained constant, i.e., if Eq. (14-9) were obeyed strictly, the 

 line representing the growth rate would be parallel to the abscissa. Let it 

 now be assumed that, on receiving each dose of ultraviolet radiation, the 

 tumor grows at a rate which is increased by an amount roughly propor- 

 tional to the dose, where the factor of proportionality may depend on the 

 past history of the course of exposures but does not change rapidly from 



' This criticism appears to extend to the hypothesis of Iversen and Arley (1953), who 

 seem to have overlooked our argument. 



