38 p. C. KOLLEK AND VALERIE WALLIS 



control value: it is 0-40 and 0-50 respectively. It can be seen that the number of 

 cells in division, 1 and 6 days after receiving 1 x 180r , is higher than in the 

 control. This increase might indicate (i) recovery from the mitosis-suppressing 

 effect of irradiation and (ii) repair process. The figures obtained from marrow of 

 of mice which received 2 x 180 r and 4 x 180 r are below the control value; 

 they seem to indicate that 1 day after this radiation dose, the duration of 

 mitosis suppression was longer than after 1 x 180 r. The interesting finding 

 concerns the higher mitotic index in the 6-day marrow samples, i.e. 1 day 

 before another fraction of 180 r was delivered, as compared with the mitotic 

 index found in the marrow of unirradiated control mice. Further investigation 

 is required to determine the statistical significance of this difference and to 

 correlate the phenomenon, if it is true, with the reduction in the number of 

 cells showing mitotic injury after three of four doses of 180 r. 



CONCLUSION 



The extensive studies of Kaplan and associates (Kaplan and Brown, 1952; 

 Kaplan et al., 1953a, b) established the fact that in mice of C57BL strain the 

 important factor in the leukaemogenic process is not the total radiation dose, 

 but the method of fractionation of the dose. The cumulative effects of frac- 

 tionated doses, which have been the subject of this preliminary report are, 

 very likely, significant contributory factors in the pre-leukaemic process. 

 Further investigation is in progress to find out how the injuries inflicted on 

 the haematopoietic system in the early stage of leukaemic transformation, are 

 contributing to the process which results in lymphoid leukaemia. 



ACKNOWLEDGMENTS 



The authors are greatly indebted to Dr. J. F. A. P. MiUer for his help and 

 to the Medical Research Council for a grant. This investigation has been 

 supported by grants to the Chester Beatty Research Institute (Institute of 

 Cancer Research: Royal Cancer Hospital) from the Medical Research Council, 

 the British Empire Cancer Campaign, the Anna Fuller Fund, and the 

 National Cancer Institute of the National Institutes of Health, U.S. Public 

 Health Service. 



EEFERENCES 



Kaplan, H. S., and Brown, M. B. (1952). J. nat. Cancer Inst. 13, 18.'). 

 Kaplan, H. S., Brown, M. B., and Paull, J. (19-5;3a). Cancer Bes. 13, 677. 

 Kaplan, H. S., Brown, M. B., and Paull, J. (1953b). J. nat. Cancer Inst. 14, 303. 

 Miller, J. F. A. P. (19G1). Advanc. Cancer Res. 6, 291. 



