Abstract
Cellular genes, termed oncogenes, are involved in the process of transformation. In a non-activated state these genes called proto-oncogenes probably play important roles in cellular growth and differentiation. In animals, the involvement of these genes in cancer is evident since retroviruses which contain activated oncogenes can be directly implicated in tumor formation (1). Some retroviruses can even activate cellular proto-oncogenes by their integration in the vicinity of such a gene (2). The evidence for proto-oncogene involvement in human cancer is more circumstantial but, nevertheless, compelling. The evidence comes from three different sources. First, DNA from human tumors can be transfected into non-transformed mouse cells and yield clones of transformed cells which contain activated human proto-oncogenes (3). Second, a high percentage of certain types of human tumors contain amplified proto-oncogenes (4,5). Third, specific chromosomal translocations are the hallmarks of certain leukemias. Proto-oncogenes have been linked to these chromosomal break-points (6,7).
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Hynes, N.E., Kozma, S., Saurer, S., Groner, B., Locher, G. (1988). An Analysis of Three Proto-Oncogenes in Primary Human Breast Tumor DNAs: The c-mos, the c-erbB-2 and the Epidermal Growth Factor Receptor Genes. In: Rich, M.A., Hager, J.C., Lopez, D.M. (eds) Breast Cancer: Scientific and Clinical Progress. Developments in Oncology, vol 56. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1753-1_1
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