Normal Tissue Development, Homeostasis, Senescence, and the Sensitivity to Radiation Injury Across the Age Spectrum
Normal Tissue Development, Homeostasis, Senescence, and the Sensitivity to Radiation Injury Across the Age Spectrum
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DOI：
10.1016/j.semradonc.2009.08.003
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发表时间：
2010-01-01
影响因子：
3.5
通讯作者：
Williams, Jacqueline P.
中科院分区：
文献类型：
--
作者：
Paulino, Arnold C.;Constine, Louis S.;Williams, Jacqueline P.
放射治疗对正常组织的后期影响因年龄而异。似乎对辐射损伤的敏感性是器官发育动态和状态的功能，它的再生潜力，最终它已经开始衰老的程度。例如，儿童的器官成熟过程可能会因放射治疗而受损甚至丧失功能，从而导致与成人不同的一系列影响，在成人中，组织修复损伤的能力和手段是慢性损伤的主要预测因素。因此，辐射引起的生长和成熟障碍是儿童所特有的，而器官损伤，在修复过程中具有组织特异性功能障碍，对儿童和成人都很常见。最后，老年人对晚期效应的易感性似乎不仅涉及他们修复损伤能力的下降，还涉及细胞磨损，所有这些都与这个年龄组中常见的共病影响交织在一起。临床医生面临的挑战是了解这些对辐射损伤敏感性的差异与年龄有关，从而制定一个调节治疗的基础，合理地减少晚期影响，最大限度地提高幸存者的生活质量。中国科学：放射科学，2010 (2):1 -2版权所有。
Late effects in normal tissues following radiotherapy vary across the age spectrum. It seems that sensitivity to radiation injury is a function of the developmental dynamics and status of the organ, its regenerative potential, and ultimately the extent to which it has begun to senesce. For instance, organ maturational processes in children can be impaired or even disabled by radiation therapy, leading to a spectrum of effects that differ from those in adults, in which the capacity and means for tissues to repair damage are the predominant predictor for chronic injury. Thus, radiation-induced impairment of growth and maturation is unique to children, whereas organ damage, with tissue-specific dysfunction in repair processes, is common to both children and adults. Finally, the susceptibility to late effects in the elderly seems to involve not only a decline in their ability to repair damage, but also cell attrition, all intertwined with effects of comorbid illness that are frequent in this age group. The challenge for clinicians is to understand these differences in the sensitivity to radiation damage with respect to age to formulate a basis for modulating therapy that can rationally minimize late effects and maximize a survivor's quality of life. Semin Radiat Oncol 20:12-20 (C) 2010 Elsevier Inc. All rights reserved.