Overview
Retroviral oncogenes originally were derived from genes in eukaryotic cells. The seminal discovery that DNA sequences within normal, uninfected, nonmalignant cells were homologous to retroviral oncogenes was made in 1976. Cellular proto-oncogenes have exon and intron structures typical of eukaryotic genes. Some exon sequences are well conserved among vertebrate and invertebrate species. The retroviral life cycle suggests a mechanism whereby cellular genes may be transduced by the viruses. The conservation of cellular proto-oncogenes among species suggests a fundamental role for them. These proto-oncogenes can be grouped according to their function or location in the cell: growth factors, growth factor receptors, nuclear proteins, and membrane proteins. The subcellular locations and functions of these proteins suggest that in normal cells they play a role in growth, development, and differentiation. Aberrant growth and development are characteristic of cancer, and the hypothesis that abnormal “activated” oncogenes contribute to the neoplastic state is therefore attractive. Changes activating normal proto-oncogenes to transforming oncogenes could occur at the DNA, RNA, or protein level. In vivo carcinogenesis is clearly a multistep process. The fact that single activated oncogenes are unable to transform normal primary cells, whereas co-introduction of at least two activated oncogenes does lead to transformation supports the genetic basis for this multistep process.
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© 1988 Springer-Verlag New York Inc.
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Burck, K.B., Liu, E.T., Larrick, J.W. (1988). Cellular Proto-oncogenes. In: Oncogenes. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-3718-1_5
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DOI: https://doi.org/10.1007/978-1-4612-3718-1_5
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