RADIATION TRANSFORMATION AND ITS MODULATION BY CHEMICALS

证据确凿地表明， 辐射或化学品（包括用于治疗 癌症）。 然而，人们对这两种因素的综合影响知之甚少。 剂. 人们可能会长期暴露在剂量下， 或多或少在他们的一生中。 虽然剂量可以预期 小，这种延长一般将涉及同期 暴露于两种或两种以上的药剂。 因此除了 预测单一病原体对公共卫生危害的不确定性 当涉及有效低剂量率下的低剂量时， 药物组合甚至更加不确定，因为潜在的 互动效应 本研究的目的是启动一个系统的研究 长期暴露的组合效应（即，多分馏或 低剂量率照射）对诱发肿瘤转化的影响 哺乳动物细胞的培养。 最初，C3 H小鼠系，命名为 10 T-1/2，将被使用，因为大量的辐射数据 暴露，或化学暴露，已经存在。 随着工作的进展， 其他动物细胞以及人类细胞将被用于建立 概括。 这项研究的最初出发点是确定 不同类别的化学品的成员（例如，直接和间接 作用诱变剂和致癌物、促进剂、反促进剂等）和 辐射（电离辐射和非电离辐射）独立发挥作用，或 交互式。 对这些测量将增加机械研究， 确定任何互动效果的性质，修复的贡献 (or错误修复）过程，以及细胞表面受体的可能作用 调节反应。 这些研究也与癌症治疗有关。 当治疗变成 更有效，寿命延长，诱发第二次的风险 肿瘤必须面对。 第二个肿瘤的诱导已经 在某些情况下有很好的记录。 这项工作可能会导致战略， 尽量减少这种风险。

The evidence is unequivocal that cancer can be induced in people by radiation or by chemicals (including those used in the treatment of cancer). However, little is known about the combined effects of these two agents. People at large can be expected to be exposed to doses protracted more or less over their lifetimes. Although the doses can be expected to be small, such protractions in general will involve contemporaneous exposures to two or more agents. Therefore, in addition to the uncertainties in predicting hazards to public health from a single agent when low doses at effectively low dose rates are involved, the risks due to combinations of agents are even more uncertain because of the potential for interactive effects. The purpose of this research is to initiate a systematic study of the combined effects of protracted exposure (i.e., multifractionation or low-dose-rate rate exposure) on the induction of neoplastic transformation of mammalian cells in culture. Initially the C3H mouse line, designated 10T-1/2, will be used since a significant amount of data for radiation exposure, or for chemical exposure, already exist. As the work progresses, other animal cells, as well as human cells, will be used to establish generalizations. The initial departure of the research will be to determine whether or not members of different classes of chemicals (e.g., directly and indirectly acting mutagens and carcinogens, promoters, antipromoters, etc.) and radiation (ionizing and nonionizing radiation) act independently, or interactively. To such measurements will be added mechanistic studies to determine the nature of any interactive effects, the contribution of repair (or misrepair) processes, and the possible role of cell-surface receptors in modulating responses. These studies are also relevant to cancer treatment. As therapy becomes more effective and lifespans are extended, the risks of inducing second tumors will have to be faced. The induction of second tumors is already well documented in some instances. This work may lead to strategies to minimize such risks.