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Genetic susceptibility to late normal tissue injury.

机译:对晚期正常组织损伤的遗传易感性。

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摘要

The outcome of all cancer therapies, including radiation, has greatly improved in the last 25 years, resulting in a doubling of the number of long-term cancer survivors. However, a subset of these survivors incurs adverse chronic side effects in unavoidably irradiated normal tissues, persisting long after treatment and compromising the quality of life of these patients. Interpatient variability in normal tissue radiation response is well documented and suggested to be under genetic control. Fibrosis, a clinically significant late effect in many irradiated tissues that results in tissue remodeling and loss of function, is a complex genetic trait making identification of the underlying genes difficult. Current clinical and animal studies are providing information on the genetics and molecular basis of late normal tissue injury in the radiation therapy setting, bringing us closer to our dual goal of individualizing treatment by genetic profiling and improving the quality of life of long-term survivors.
机译:在过去的25年中,所有癌症疗法(包括放射疗法)的结果都得到了极大的改善,从而使长期癌症幸存者的数量增加了一倍。然而,这些幸存者中的一部分在不可避免的受辐照的正常组织中产生不利的慢性副作用,在治疗后持续很长时间,并损害了这些患者的生活质量。患者间正常组织放射反应的变异性已得到充分证明,并建议在基因控制下进行。纤维化是许多受辐照组织在临床上的显着晚期效应,可导致组织重塑和功能丧失,是一种复杂的遗传特征,难以识别基础基因。当前的临床和动物研究正在提供有关放疗中晚期正常组织损伤的遗传学和分子基础的信息,这使我们更接近通过基因谱分析个性化治疗并改善长期幸存者生活质量的双重目标。

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