Abstract
The two basic premises upon which investigation of the malignant phenotype is based are that malignancy results via alterations in the genetic material of the cell, and that the accumulation of these alterations occurs in a multistep fashion. Early indication that normal cellular genes were the targets for mutation came from the observation that the acutely transforming retroviruses contained abnormal copies of cellular genes (the protooncogenes), the presence of which was required for the transforming activity of the viruses [reviewed in J. M. Bishop (1983)]. Over three dozen protooncogenes have been identified through transfection by retroviruses, gene transfection, and homology to retroviral oncogenes (J. M. Bishop, 1985; ‘Rhim, 1988). These activated oncogenes tend to be dominant, their activity overriding that of the normal allele. The multistage hypothesis was supported byin vitrostudies demonstrating that the conversion of primary cells from the normal to the tumorigenic phenotype requires a minimum of two cooperating oncogenes (Land et al., 1983) and from epidemiological studies of human cancer which suggested that two to seven steps were required before cancer was manifestedin vivo(Armitage and Doll, 1954; Ashley, 1969b; Nordling, 1953).
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Goddard, A.D., Solomon, E. (1993). Genetic Aspects of Cancer. In: Harris, H., Hirschhorn, K. (eds) Advances in Human Genetics 21. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3010-7_4
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