CHANGES IN EARLY AND LATE RADIATION RESPONSES WITH ALTERED DOSE FRACTIONATION - IMPLICATIONS FOR DOSE-SURVIVAL RELATIONSHIPS
CHANGES IN EARLY AND LATE RADIATION RESPONSES WITH ALTERED DOSE FRACTIONATION - IMPLICATIONS FOR DOSE-SURVIVAL RELATIONSHIPS
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DOI：
10.1016/0360-3016(82)90517-x
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发表时间：
1982-01-01
影响因子：
7
通讯作者：
FLETCHER, GH
中科院分区：
文献类型：
--
作者：
THAMES, HD;WITHERS, HR;FLETCHER, GH
剂量分次变化后正常组织早期和晚期辐射反应的不同变化的临床和实验证据表明，后期反应对每部分剂量变化的敏感性更高。在实验研究的影响，剂量每部分的早期和晚期isoeffects，一个较大的分数指数的晚期反应的规则。这些发现意味着，其耗竭导致迟发效应的靶细胞的剂量-存活曲线的形状与急性效应的靶细胞不同;随着剂量增加，相对于单次击中事件的杀伤，累积亚致死损伤对细胞杀伤的贡献在迟发效应的靶细胞中增加得更快。晚期损伤的靶细胞存活曲线必须比急性效应的曲线更弯曲。尽管这样的存活曲线特征与选择来描述它们的存活曲线模型无关，但是它们将代表，就线性二次模型的参数而言，S = e-α D-β D2，更高的β/。α的延迟效应的比率。如果肿瘤克隆原的剂量存活特征类似于急性反应正常组织中的靶细胞的那些，并且如果正常组织中的晚期损伤是剂量限制性的，则通过超分割降低每部分的剂量大小将导致治疗增益。相反，增加每部分的剂量大小应减少治疗差异。
Clinical and experimental evidence for divergent changes in early and late radiation responses in normal tissues after changes in dose fractionation indicate a greater sensitivity of later responses to changes in dose per fraction. In experimental studies of the effect of dose per fraction on early and late isoeffects, a larger number-of-fractions exponent for the late responses is the rule. These findings imply that the shape of the dose-survival curve for the target cells whose depletion results in late effects is different from that for target cells for acute effects; as the dose increases the contribution to cell killing from accumulated sublethal injury, relative to killing from single hit events, increases more rapidly in the target cells for the late effects. The survival curve for the target cells for late injury must be curvier than that for acute effects. Although such survival curve characteristics are independent of the survival curve model chosen to describe them, they would represent, in terms of the parameters of the linear quadratic model, S = e-.alpha.D-.beta.D2, a higher .beta./.alpha. ratio for late effects. If the dose survival characteristics of tumor clonogens resemble those of the target cells in acutely responding normal tissues, and if late injury in normal tissues is dose-limiting, a therapeutic gain would result from reducing the size of dose per fraction by hyperfractionation. Conversely, increasing the size of dose per fraction should reduce the therapeutic differential.