ABSTRACT: Early studies designed to investigate the molecular basis of oncogenesis indicated the existence of discrete genes which could cause neoplastic transformation of normal cells in vitro. These genes (which became known as oncogenes) were originally thought to be derived from oncogenic retroviruses and neoplastic transformation was believed to be the result of infection of normal cells by an oncogenic retrovirus. However, recent studies have demonstrated that normal eukaryotic cells contain gene sequences which are highly homologous to oncogenes but which do not cause neoplastic transformation. These genes (termed proto-oncogenes) have been found to code for proteins which are intimately involved in the regulation of mitosis. These include growth factors, receptors for growth factors, proteins (such as protein kineses and GTP binding proteins) which transduce exogenous signals through the plasma membrane, and nuclear binding proteins. Thus, if the function or control of a proto-oncogene (or its product) is altered by mutation, gene rearrangement, or translocation, its effects on the cell will also change. This, in turn, can lead to the loss of normal mitotic control. The tumorigenic process is, of course, much more complicated that just unchecked cell growth. However, the insights into the molecular basis of cellular regulation have suggested new approaches to the early diagnosis of cancer and may ultimately lead to the development of more effective treatment protocols.