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Yoshida sarcoma cells, which have the same growth characteristics as ascites cells in the mouse and in cell suspension, were partially synchronized in vitro by means of excess thymidine (0.1 mM thymidine for 18 h). The growth of non-synchronized cultures was inhibited by irradiation, the degree depending on the dose of radiation. At the same time, a 50% inhibition in vivo (380 rad) and in vitro (480 rad) was determined. The incorporation of 3H-thymidine into the DNA is inhibited by 10-32%, depending on the radiation dose. The mitotic index decreases 2 h after irradiation by a dose-dependent amount. A mitotic maximum develops later; the delay is dose-dependent. Partially synchronized cells were irradiated in the G1/S-, G2-, and G1-phase. As compared to the 3H-thymidine incorporation and the mitotic index there were no significant differences between the cultures which were irradiated in the individual phases of the non-synchronized control cultures. The cultures which were irradiated in the G2-phase, however, showed a significantly reduced growth in vivo after 48 h. If the cells were cultured for more than 72 h after irradiation, the differences between the cultures irradiated in the G2-phase and the other phases were reduced.

The effect of local irradiation of a rapidly metastasizing sarcoma in the leg of the rat was measured in terms of (a) regression of the primary tumour and (b) growth of metastases produced in lymph nodes and lungs, by dissemination occurring after irradiation of the primary tumour. These effects on rats which had been irradiated while breathing air were compared with rats breathing 10% O(2)/90% N(2) in which a tourniquet had been applied proximal to the tumour to arrest blood flow during irradiation. Tourniquet anoxia increased radioresistance of growth of primary tumour by (OER) factors of 2·9-3·3. Corresponding factors for inhibition of growth of metastases in abdominal lymph nodes, and for the reduction in incidence of lung metastases produced by single tumour cells, were 2·7 and 2·4 respectively. These results suggest that this tumour was radiobiologically well oxygenated when it was irradiated in a poorly vascularized stage of growth where tumour necrosis had developed.