Normal tissue responses to ionizing radiation have been a major subject for study since the discovery of X-rays at the end of the 19th century. Shortly thereafter, time-dose relationships were established for some normal tissue endpoints that led to investigations into how the size of dose per fraction and the quality of radiation affected outcome. The assessment of the radiosensitivity of bone marrow stem cells using colony-forming assays by Till and McCulloch prompted the establishment of in situ clonogenic assays for other tissues that added to the radiobiology toolbox. These clonogenic and functional endpoints enabled mathematical modeling to be performed that elucidated how tissue structure, and in particular turnover time, impacted clinically relevant fractionated radiation schedules. More recently, lineage tracing technology, advanced imaging and single cell sequencing have shed further light on the behavior of cells within stem, and other, cellular compartments, both in homeostasis and after radiation damage. The discovery of heterogeneity within the stem cell compartment and plasticity in response to injury have added new dimensions to the consideration of radiation-induced tissue damage. Clinically, radiobiology of the 20th century garnered wisdom relevant to photon treatments delivered to a fairly wide field at around 2 Gy per fraction, 5 days per week, for 5-7 weeks. Recently, the scope of radiobiology has been extended by advances in technology, imaging and computing, as well as by the use of charged particles. These allow radiation to be delivered more precisely to tumors while minimizing the amount of normal tissue receiving high doses. One result has been an increase in the use of schedules with higher doses per fraction given in a shorter time frame (hypofractionation). We are unable to cover these new technologies in detail in this review, just as we must omit low-dose stochastic effects, and many aspects of dose, dose rate and radiation quality. We argue that structural diversity and plasticity within tissue compartments provides a general context for discussion of most radiation responses, while acknowledging many omissions. © 2020 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

中文翻译：

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辐射引起的组织损伤和反应。


自 19 世纪末发现 X 射线以来，正常组织对电离辐射的反应一直是研究的主要课题。此后不久，针对一些正常组织终点建立了时间-剂量关系，从而研究了每部分的剂量大小和放射质量如何影响结果。 Till 和 McCulloch 使用集落形成测定法评估骨髓干细胞的放射敏感性，促使建立了针对其他组织的原位克隆形成测定法，这些测定法已添加到放射生物学工具箱中。这些克隆形成和功能终点使得能够进行数学建模，阐明组织结构，特别是周转时间，如何影响临床相关的分割放射计划。最近，谱系追踪技术、先进成像和单细胞测序进一步揭示了干细胞和其他细胞区室中细胞在稳态和辐射损伤后的行为。干细胞区室内异质性和响应损伤的可塑性的发现为考虑辐射引起的组织损伤增加了新的维度。在临床上，20 世纪的放射生物学积累了与光子治疗相关的智慧，光子治疗以每次 2 Gy 左右、每周 5 天、持续 5-7 周的方式传递到相当广泛的视野。最近，由于技术、成像和计算的进步以及带电粒子的使用，放射生物学的范围得到了扩展。这些可以使辐射更精确地传递到肿瘤，同时最大限度地减少接受高剂量的正常组织的数量。 一个结果是越来越多地使用在更短的时间内给予更高剂量的每次分割（大分割）。我们无法在本次综述中详细介绍这些新技术，就像我们必须忽略低剂量随机效应以及剂量、剂量率和辐射质量的许多方面一样。我们认为，组织室内的结构多样性和可塑性为讨论大多数辐射反应提供了一般背景，同时承认许多遗漏。 © 2020 作者。 《病理学杂志》由 John Wiley & Sons Ltd 代表大不列颠及爱尔兰病理学会出版。