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ON THE RATE OF INCIDENCE OF MALIGNANT TUMORS H. S. ANKER, M.D., Ph.D.* Most investigators at present seem to favor the view that the change ofa normal body cell into a tumor cell is a rare event and that, in general, once such a change has taken place, a macroscopic tumor develops. This assumption is quite independent ofthe nature ofthe causal agents responsible for the changes themselves (1-6). As an alternative, I propose that the change ofa normal body cell into a tumor cell is a relatively frequent event—a hypothesis which is also not concerned with the causal agents involved in the genesis of tumor cells. A number ofconsequences follow from this hypothesis which appear to be testable and therefore might be of some value in the field of tumor research . They are as follows: i. If the generation of a tumor cell is a frequent event, means which normally protect the organism from the malignant cells have to be postulated . Two alternatives can be visualized: either a tumor cell is dependent on its surroundings for growth (latent cells) so that only occasionally is the continued maintenance ofthe tumor cell and its descendants promoted; or the organism is normally capable ofrestraining the growth of, or destroying , the tumor cells by a specific defense mechanism, which on occasion fails to function. For want ofa better term, I shall call either ofthese means a "protection system." This system could operate either on a local or a systemic level, and only in those rare cases in which a protection system fails to operate, can an altered cell develop into a macroscopic tumor. Reactivation ofan ineffective protection system may be involved in the spontaneous remission of tumors. From the therapeutic point of view, it appears attractive to visualize the possibility ofbeing able to restore an im- * Department ofBiochemistry, University ofChicago. 436 H. S. Anker · Tumor-Cell Rate Perspectives in Biology and Medicine · Summer ic paired protective mechanism rather than to have to rely on the relatively small differences between normal and tumor cells with respect to X-rays, metabolic antagonists, etc. (7). A number ofagents—such as X-rays, for example—damage a far greater number ofcells than subsequently develop into manifest tumors. This observation supports the notion ofa system whose normal function is to take care ofabnormal or damaged cells. Similarly, local stressnot only may be a causal agent for the development oftumors but may also damage the protection system. At present it is not possible to identify the postulated system with any of the known defense mechanisms available to the mammalian organism. In particular, the relation of the protection devices to immunological responses (8) remains to be determined; and it also remains to be seen what, if any, similarity there is between such a protection system and the mechanism by which an organism rids itself of over-age erythrocytes (9). 2.As a first approximation, it could be assumed on the basis of such a hypothesis that the rate ofcell alteration is proportional to the rate ofcell division, and it could be concluded, therefore, that the rate ofcell alteration decreases with increasing age. It could be further assumed that the efficiency ofthe protection mechanism will decrease with increasing age, as do all otherfunctions ofthe body. The absolute rates ofthe two processes, however, will be different. It seems possible that these rates could be estimated approximately from the rates ofcell division and oftissue-damage repair; a mathematical expression involving the two rates could then be arrived at which should yield the rate oftumor incidence as a function of age. Once such a correlation is established, it might become the basis on which the rate oftumor incidence could be related to one ofthe proposed causal agents ofcell alteration. 3. It further follows from such a hypothesis that it might prove possible to prevent the development ofmanifest tumors by methods which preserve the efficiency ofthe normal body organization that protects against altered cells instead ofby methods which inhibit the action ofthe causal agents. While I cannot at present advance experimental data to support this hypothesis, other than to point to the literature on cancer research, perhaps a search along these lines...


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