ABELSON LEUKEMIA VIRUS TRANSFORMATION

大量的逆转录病毒高频率地诱发肿瘤 当注入到适当的宿主中时。 大多数病毒通过 直接干扰正常细胞生长， 分化，因为它们也在体外转化细胞， 可以在受控条件下研究细胞-病毒相互作用。 几乎所有这些转化病毒都携带衍生自 从正常细胞的DNA中分离出来， 负责细胞转化的蛋白质。 因为 onc基因来自正常细胞DNA，理解 它们在病毒系统中的作用方式将是重要的一步 不仅在肿瘤发生中， 正常的生长和发育。 我们正在研究这个 使用Abelson病毒（A-MuLV）模型系统和 遗传方法。 A-MuLV转化了一些成纤维细胞， 小鼠淋巴肉瘤。 通过分离变异体A- MuLV毒株，已经有可能分离病毒功能 成纤维细胞和淋巴转化所需的，以及 高效淋巴转化所需的那些， 体外和体内。 我们计划利用这些变种人并隔离其他变种人 确定控制A-MuLV细胞的机制 互动

A large number of retroviruses induce tumors at high frequency when injected into appropriate hosts. Most of these viruses act by directly interfering with normal cellular growth and differentiation and, because they also transform cells in vitro, the cell-virus interactions can be studied under controlled conditions. Nearly all of these transforming viruses carry gene(s) derived from normal cellular DNA called onc genes that encode the proteins that are responsible for cellular transformation. Because onc genes are derived from normal cellular DNA, understanding their mode of action in a viral system would be an important step toward understanding their role, not only in oncogenesis but also in normal growth and development. We are examining this question using a Abelson virus (A-MuLV) model system and a genetic approach. A-MuLV transforms some fibroblast of lymphosarcomas in mice. Through the isolation of variant A- MuLV strains, it has been possible to separate viral functions required for fibroblast and lymphoid transformation as well as those required for high efficiency lymphoid transformation in vitro and in vivo. We plan to use these mutants and isolate others to determine the mechanism(s) that control A-MuLV-cell interaction.