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Part of the book series: Cancer Treatment and Research ((CTAR,volume 63))

Abstract

The v-myc oncogene was first identified in 1977 as the transforming gene of the MC29 avian retrovirus, which causes myelocytomatosis, carcinomas, and sarcomas in chickens [1]. The c-myc proto-oncogene has since been identified in a wide variety of organisms ranging from the invertebrate sea star [2] to humans [3]. Deregulated expression of a normal c-myc gene leads to malignant transformation in certain cell culture models, such as primary rat embryo fibroblasts (REF; in which the coexpression of a second activated oncogene, ras, is also required) [4,5], and in transgenic mice [6] and rabbits [7]. Burkitt lymphoma, a naturally occurring human tumor, provides a paradigm for the role of c-myc in malignant transformation. In this case, chromosomal translocation of the c-myc locus to a location downstream of the regulatory elements of the immunoglobulin heavy chain gene results in deregulated expression of c-myc [8]. In contrast to many other oncogenes that have activating mutations in the coding sequence, this deregulated expression of a normal c-myc coding sequence appears to be responsible for the oncogenic contribution of c-myc [4].

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Kato, G.J., Wechsler, D.S., Dang, C.V. (1993). DNA binding by the Myc oncoproteins. In: Benz, C.C., Liu, E.T. (eds) Oncogenes and Tumor Suppressor Genes in Human Malignancies. Cancer Treatment and Research, vol 63. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3088-6_16

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  • DOI: https://doi.org/10.1007/978-1-4615-3088-6_16

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