WORLD MALARIA SITUATION

issue, Professor E. S. Finckh gives his reasons for believing that somatic mutation need not always underlie the altered cellular appearances and behaviour of tumours, and that features of neoplasia may sometimes represent acquired errors in cellular differentiation. This concept is cogent and worthy of consideration. In particular, Finckh points out that cellular features that are usually taken to be characteristic of tumours are, in fact, normal in other cells of the body from time to time. The list he gives includes frequent mitoses, as occur normally in bone marrow and intestinal mucosa; local invasion of adjacent tissues, as by fibroblasts and endothelial cells in repair; widespread dissemination of a single cell type to remote parts of the bodr, as occurs with leucocytes; the production of hormones that are normal in other tissues; and the presence of oncofetal antigens that are normal in early development. He also suggests that the principal histological abnormalities that are used for the diagnosis of cancer, such as large, hyperchromatic and hence usually aneuploid nuclei, may well be the result and not the cause of the increased cellular multiplication that goes with the tumorous state; and that, although these features are very helpful in diagnosis, it is not surprising that they may also lead to error, occurring as they sometimes do in rapidly growing non-neoplastic conditions. Another point made by Finckh is that the dividing lines between hytlerplasias and atypias on the one hand and tumours on the other are obscure; this would not be expected if tumours were the result of clonal proliferation of single mutant cells, but would be expected if the changes resulted from inductive actions upon fields of cells. He goes on to suggest that this concept would not only fit the pathologists' experience with tumours rather better, but would also explain the otherwise confusing overlap with nodular hyperplasias and focal metaplasias, as all might then be seen as part of a single general process of heritable but extragenetic cellular aberration. Finally, he concludes that were abnormal differentiation rather than somatic mutation to account for neoplasia, at least in the early stages of some tumours, then the search for therapeutic measures against cancer ought not only to include the exploitation of differences from normal cells, but also the use of agents that might either reverse or extend the aberrant forms of differentiation in the tumour cells. The argument presented is almost Lamarckism versus Darwinism all over again-the inheritance of acquired characteristics (as occurs after organ induction in the embryo) as against the natural selection of mutants. It is certainly to be hoped that these views will receive critical attention and, in turn, challenge, for it is only by the testing of such new ideas that cancer research can be made to advance.