Abstract
Histopathological observations of the development of tumors have led to the concept that oncogenesis proceeds through the sequential acquisition of independent growth-related phenotypic characteristics (Foulds 1975). This process of tumor progression occurs through events involving the expression of specific genes affecting the regulation of cellular growth (recently reviewed in Weinberg 1985; Klein and Klein 1985; Bishop 1985). The requirement of two complementing oncogenes for the in vitro transformation of primary rat embryo firbroblasts provides a useful in vitro experimental model of tumor progression. Ha-ras (EJ) and v-myc or Ha-ras (T24) and E1A can act together to transform primary fibroblasts, while neither oncogene acting alone is capable of causing efficient transformation (Land et al. 1983; Ruley 1983) unless expressed at a high level (Spandidos and Wilkie 1984).
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© 1986 Springer-Verlag Berlin · Heidelberg
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Schwartz, R.C., Stanton, L.W., Marcu, K.B., Witte, O.N. (1986). An In Vitro Model for Tumor Progression in Murine Lymphoid Cells. In: Melchers, F., Potter, M. (eds) Mechanisms in B-Cell Neoplasia. Current Topics in Microbiology and Immunology, vol 132. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-71562-4_10
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DOI: https://doi.org/10.1007/978-3-642-71562-4_10
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