Effect of colchicine injection prior to the initiating phase of two-stage skin carcinogenesis in mice.

Colchicine injected 5, 9 and 24 h respectively before initiation (using s.c. injection of urethane for initiating action and TPA skin applications for promoting action, in female ICR mice) led to a significant increase in skin tumour incidence in the --9-h group, and an increase in percentage malignancy in both the --5- and --9-h groups. These times corresponded to the peak of metaphase arrest by the colchicine. The results are discussed in relation in those of Pound and Withers (1963) and others, who found that mitotic stimulation at the time of urethane initiating action raised the ultimate tumour incidence; and the inference is drawn that initiating action in mouse skin may occur during the M phase, rather than during the G1, S, or G2 phases, as suggested by others

Failure of syngeneic bone marrow cells to protect against MC-induced lymphoma in dba-2 mice.

IT has been shown long ago that shielding the bone marrow (Kaplan and Brown, 1951) or spleen (Lorenz et al., 1953) of mice during exposure to whole-body X-irradiation, or injection of syngeneic bone marrow cells after whole-body irradiation (Kaplan et al., 1953), reduces the incidence of thymic lymphomas resulting from the irradiation. How the effect is brought about has never been satisfactorily explained. There is presumably some essential factor in the normal hematopoietic system which irradiation is able to depress. Whether this inhibitory process affects a specific stage in radiation leukaemogenesis, or whether it is concerned with the leukaemogenic process as such, irrespective of the nature of the leukaemogenic agent, has not so far been fully established. Indirect evidence would suggest, however, that the former (i.e. a specific anti-radiation effect) is the more likely explanation. It is known, for instance, that bone marrow cells of C3H mice, though acceptable to tolerant AKR mice, fail to inhibit the spontaneous development of thymic lymphomas in the latter strain (Miller, 1960). In the case of leukaemogenesis b