| Literature DB >> 7826840 |
Abstract
The dramatic nature of radiation-induced spinal cord injury causes clinicians to avoid doses that could lead to this complication, sometimes even to the point of possibly compromising tumor control. As a consequence, clinical data on radiation myelopathy are limited. So far, experimental investigations have been devoted to establishing the dose-response, time-dose-fractionation relationships, and volume effects for CNS injury in various animal models. Concepts and parameters gained from such laboratory studies have been useful for the development of new radiotherapy strategies in terms of dose fraction schedules and dose adjustments as a function of radiation volumes. Further advances in therapeutic strategies, however, must come from elucidation of the pathogenesis of radiation-induced CNS injury. Results of recent studies warrant revision of the current concept that such injuries result simply from reproductive killing of glial "stem cells" and endothelial cells. Emerging evidence indicates that various cell types contribute to determining the progression of radiation lesions.Entities:
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Year: 1994 PMID: 7826840
Source DB: PubMed Journal: Oncology (Williston Park) ISSN: 0890-9091 Impact factor: 2.990