Over the past 4 years, we have developed a new method of studying the role of viral gene functions in the tumorigenicity of virus transformed cells. This method is based on quantitative analysis of the tumor inducing capacity of DNA virus transformed cells in animals that possess different capacities to mount cellular immune, antitumor defenses. For this method, the relationship between transformed cell dose, tumor incidence and time of tumor appearance (tumor latency) is determined repetitively for clones of rodent embryo cells transformed by different viruses. By expressing the transformed cell dose - tumor incidence data as the mean of the tumor producing dose 50% end point (TPD50) and the transformed cell dose - tumor latency data as the average tumor latency, an objective characterization of the tumorigenicity (i.e. tumor inducing capacity or tumorigenic phenotype) of any particular transformed cell clone can be obtained. Significant differences in mean TPD50 values or average tumor latencies of the same cells in different types of tumor challenged hosts identifies the specific traits of tumor cells that may be induced by viral gene functions. Differences in these data among cell lines transformed by different viruses in different types of hosts permits identification and classification of the different viral gene functions that are putatively involved in transformed cell tumorigenicity. Standard statistical analyses of such data have proven to be inadequate. Attempts are underway to develop alternative statistical approaches.
