An In Vitro Model for Tumor Progression in Murine Lymphoid Cells
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).
KeywordsSlot Blot Cell Neoplasia Soft Agar Medium Adherent Bone Marrow Murine Plasmacytoma
Unable to display preview. Download preview PDF.
- Foulds L (1975) Neoplastic development, Vol 2. Academic Press, LondonGoogle Scholar
- Potter M, Wiener F, Mushinski JF (1984) Recent developments in piasmacytomagenesis in mice. Viral Oncology 4: 139–162Google Scholar
- Schwartz RC, Stanton LW, Riley SC, Marcu KB, Witte ON (1986) Synergism of v-myc and v-Ha-ras in the in vitro neoplastic progression of murine lymphoid cells. SubmittedGoogle Scholar