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CELLS in mitosis, or preparing for mitosis, have proved susceptible to a wide range of compounds. Encouragement to continued efforts to find more effective anti-mitotics has come from the ability of existing agents to achieve the frequent cure of some patients with gestational choriocarcinoma, the less regular cure of patients with some other uncommon solid tumours, and a high rate of temporary remission in many leukaemias. Except for this relatively small range ofneoplasms, aniti-mitotics have so far been found to have only limited value. It is recognised that to be more effective they require an additional basis for selective action against tumour cells (Haddow, 1963) but in general their failure has been attributed to the development of resistance operating through the classical mechanisms of variation and selection (Law, 1956; Potter, 1958; Klein, 1961; Welch, 1965). The general feasibility of controlling tumour growth and of eliminating tumours with anti-mitotic agents, in the absence of classical drug resistance, has received little attention and it is the purpose of this paper to examine this question. Tumour growth has been studied in terms of change of volume as a function of time and in terms of cell proliferation kinetics. The less studied inter-relationship of these two functions is central to our understanding of tumour growth but it is complicated by two factors. One is that some tumour cells die and the other is that tumours do not usually consist exclusively of fertile or proliferative tumour cells (Table I). A consideration of this inter-relationship precedes the present analysis of anti-mitotic action.

Tumour growth and anti-mitotic action. The role of spontaneous cell losses