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The mos oncogene has been useful for studying oncogene/proto-oncogene function and has provided unique insight into the molecular basis of neoplastic transformation. Like many other oncogenes, mos was discovered as part of the acute transforming retrovirus Moloney murine sarcoma virus (Mo-MSV). Mo-MSV is a replication-defective virus that causes fibrosarcomas in mice, rats, and hamsters (1-3). Reviews of the properties of Mo-MSV have been published (4,5). Early studies with Mo-MSV (6) described what is now referred to as the toxicity of acute infection. A large percentage of fibroblasts infected with Mo-MSV round up and show evidence for premature chromatin condensation, ring chromosome formation, and chromosome pulverization (7). The floating cells do not proliferate, while the cells that remain attached typically develop as foci of disoriented spindle-shaped transformed cells (8). These transformed cells are anchorage independent, grow in semisolid media to high saturation density, and show a disruption of the cytoskeleton, all of which are changes observed with other transformed cells and transforming genes. Papkoff et al. (9) demonstrated that cells acutely infected with Mo-MSV express a 30- to 100-fold higher level of mos product than stably transformed cell populations (10, 11). The recent discovery that the mos proto-oncogene product is cytostatic factor (CSF) suggests that toxicity during acute infection is due to CSF activity caused by high levels of Mo-MSV mos product (12). |
