ABELSON LEUKEMIA VIRUS TRANSFORMATION

大量逆转录病毒高频率诱发肿瘤 当注入适当的宿主时。这些病毒中的大多数都通过 直接干扰正常的细胞生长和 分化，因为它们也会在体外转化细胞，所以 细胞与病毒的相互作用可以在受控条件下进行研究。 几乎所有这些转化病毒都携带S衍生的基因 来自正常的细胞DNA，称为onc基因，编码 负责细胞转化的蛋白质。因为 ONC基因来自正常细胞DNA，理解 他们在病毒系统中的行动模式将是重要的一步 了解它们的作用，不仅在肿瘤发生中，而且在 在正常的生长和发育中。我们正在研究这件事 使用Abelson病毒(A-MuLV)模型系统和 遗传方法。A-MuLV转化成纤维细胞 小鼠的淋巴肉瘤。通过分离变异体A- MuLV毒株，已经有可能分离病毒功能 成纤维细胞和淋巴样转化所必需的 高效淋巴转化所需的条件 体外和体内。我们计划利用这些突变体并分离出其他突变体 控制A-MULV细胞的机制(S)的确定 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.