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1 Origins of Contemporary RNA Tumor Virus Research


Most, if not all, complex eukaryotic organisms are subject to disorders of cell growth and differentiation that result in the appearance of localized or disseminated tumors. Although a large number of physical, chemical, and biological agents have been implicated in the etiology of neoplastic growth (Hiatt et al. 1977), it is generally agreed that some stage of tumorigenesis usually involves specific genetic alterations in individual cells whose progeny constitute the tumor mass (Cairns 1975Cairns 1980). Those genetic alterations may be multiple (Armitage and Doll 1957), they may be inherited (Ponder 1980), or they may be induced or contributed by some of the agents implicated in tumorigenesis. Such a statement implies that the etiology of cancer is complex, a view that is reinforced by the study of the pathology and clinical behavior of tumors arising in the many cell lineages in higher organisms.

The great attraction of oncogenic viruses for experimentalists interested in cancer depends in large part on the apparent simplicity of many of these agents and on the correlative hope that a detailed understanding of the genetic contribution such viruses make to a cell will enlarge our understanding of neoplastic conversion in general. In the happiest of all experimental situations, a virus introduces into a normal cell a single gene whose product is capable of initiating and maintaining the oncogenic state. This state of affairs appears to apply to some viral agents, prompting a number of immediate questions to which at least partial answers are now available: Where...

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