Abstract
The mechanisms of virus-host cell interaction resulting in the transformation of normal cells to neoplastic cells has been examined in several systems. Elegant experiments with the SV40-3T3 mouse fibroblast system reported by Todaro and Green (1) demonstrated that active cell replication and DNA synthesis are required to fix the transforming event between virus and target cell. Stoker (2) observed that the frequency of transformation of polyoma virus was increased among BHK-21 hamster cells which have survived X-irradiation. Exposure of mouse fibroblast cells to radiomimetic thymidine analogues enhanced the efficiency of SV40 transformation fivefold (3). Borek and Sachs observed that 300 R of X-irradiation induced the in vitro transformation of hamster embryo cells when cultured on mouse cell feeder layers (4). Processes associated with cell replication were essential soon after irradiation to fix the transformed state (5). A hereditary and a physiological state of susceptibility to transformation appeared to exist in X-irradiated cells and mechanisms for repair of radiation damage (“error correction”) directly controlled the development of the transformed state (6).
Recent studies in this laboratory demonstrated that exposure of primary hamster embryonic cells to 150 R of X-irradiation prior to infection produced a 15- to 50-fold increase in the number of transformed clones when compared with unirradiated controls (7). Radiation alone under these conditions did not produce transformed cells. Characterization of the radiation responses of normal embryonal cells in culture is fundamental to understanding the role of irradiation in sensitizing these cells to transformation by SV40 virus. The present report describes results obtained in the investigation of several parameters of radiation induced changes in normal hamster cells in culture. A parallel study was conducted on the radiation response of SV40 transformed isogenic hamster cells to define potential viral induced changes that may exist.
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