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RADIATION BIOLOGY 



initial period of exposures was followed by a rest period of 30 days, after 

 which the exposures were resumed for another period. In some cases 

 there was another terminal rest period, because it became necessary to 

 discontinue the whole experiment. A^ain the calculated values of td 

 gi\en in Table 14-5 dilTer somewhat from the ob.scrved values, the 

 observed being generally greater than the calculated. The discrepancies 

 seem to be in the same direction as those that result when comparisons 

 of the data for different dosage intervals are considered. All in all, these 

 discrepancies do not seem too important when it is realized that our 

 treatment has been based on a crude model. Figure 14-5, which describes 

 this model, certainlj^ does not accurately describe actual tumor growth; 

 it is hardly to be believed that the growth rate rises immediately on the 

 application of ultraviolet radiation as is indicated in that diagram. 



Table 14-5. Effect of Interrupting Schedule ok Doses 

 (From Blum, 1950b.) 

 For all experiments, data are for 50 per cent incidence; D = 2.0; / = 1.4. This is the 

 experiment described in Fig. 14-9. All series were run simultaneously. 



Series 



DK 

 DI. 

 DG 

 DE. 

 DC. 

 DA. 



td (observed; td (calculated) 



155 

 169 



180 

 189 

 191 

 200 



155 

 170 

 173 

 176 

 178 

 181 



* Periods without exposures. 



As regards the more intimate aspects of carcinogenesis by ultraviolet 

 radiation there is relatively little to say. The active hyperplasia which 

 results from sunburn, and which is also very marked in mouse skin sub- 

 jected to ultraviolet radiation (Grady et al., 1941), attracts attention and 

 suggests that the same or a similar primary mechanism is involved. It is 

 obvious that some acceleration of cell proliferation is involved in cancer 

 development whether or not it is of the progressive type suggested. In 

 this respect it is interesting that there is no real evidence of acceleration 

 of cell division due to the direct effect of ultraviolet radiation on the cell, 

 but only retardation (see Giese, 1947; Blum and Price, 1950). Such evi- 

 dence does not eliminate the possibility of indirect effects (see Hollaender 

 and Duggar, 1938; Loofl)ourow and Morgan, 1940). 



The idea that a steroid is changed by ultraviolet radiation into a car- 

 cinogen was for a time popular. Roffo, who thought cholesterol was the 

 precursor, seems to have been the first to propose this. Various investi- 

 gators, using a variety of approaches, failed, however, to find evidence to 

 support this idea (see Blum, 1940, for numerous references). Studies on 



