ONCOGENESIS FROM LOW-DOES-RATE X-IRRADIATION

我们的目的是获得关于致癌基因频率的信息， 变换作为曝光时间的显式函数， 剂量率对长期照射后残留的潜在转化损害的影响 X射线照射 这种潜在的损伤及其通过启动子的表达 12-0-十四烷酰基-佛波醇-13-乙酸酯将通过慢性 TPA-用高剂量率递送的X射线开始的细胞治疗，或 持续时间长达8 h。 我们将继续使用来自小鼠细胞的C3 H/10 T1/2细胞系 其中，通过对堆积在 融合单层。 实验将在37摄氏度下进行， 积极培育文化。 我们将继续使用持续曝光 时间技术的细胞照射在减少剂量率。 在 累积或急性剂量为0.25至4戈伊，我们将分析 立即开始用0.1 μ g/ml TPA处理X射线引发细胞 在愤怒之后。 对照组（不含TPA但含TAP溶剂） 将遵循同样的程序。 相关因素将根据 长期暴露的转化频率与 从急性暴露（4戈伊/min）到相同剂量的时间T到频率， 有或没有TPA与（a）剂量，以获得信息的 修复过程的效率，或（B）总曝光时间，以获得 修复过程的动力学信息。

Our aim is to obtain information on the frequency of oncogenic transformation as an explicit function of exposure time for a variety of dose rates on latent transformation damage remaining after protracted X-irradiation. This latent damage and its expression by the promoter 12-0-tetradecanoyl-phorbol-13-acetate will be investigated by chronic TPA-treatment of cells initiated with X-rays delivered at high dose rate or protracted over times up to 8 h. We will continue to use the C3H/10T1/2 cell line derived from mouse cells in which transformation is quantitated by scoring piled-up foci on top of a confluent monolayer. Experiments will be performed at 37 degrees C with actively growing cultures. We will continue to use a constant exposure time technique for cellular irradiation at reduced dose rates. At cumulative or acute doses of .25 to 4 Gy, we will assay the population of X-ray initiated cells by TPA-treatments at 0.1 Mug/ml beginning immediately after irratiation. The control groups (without TPA but with TAP-solvent) will follow the same procedure. Relative factors will be estimated from the ratio of the transformation frequencies from protracted exposures over time T to frequency from an acute exposure (4 Gy/min) to the same dose, with or without TPA versus (a) the dose to obtain information on the efficacy of rapair processes, or (b) the total exposure time to obtain information on the kinetics of repair processes.