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随着肿瘤患者的逐年增加,接受放疗的患者也在不断增加。2012年,全球新增癌症病例1400多万例,中国每年新增肿瘤患者300多万例,而肿瘤患者中约有70%接受放射治疗,这些患者接受治疗的远期效应会影响患者的生活质量[1]。造血系统对辐射高度敏感,在接受照射后造血干细胞(hematopoietic stem cell,HSC)会出现凋亡、衰老或者分化等损伤性改变,引起造血系统应激能力下降,导致肿瘤患者长期骨髓抑制[2]。现将辐射诱导长期骨髓抑制的有关研究综述如下。
辐射导致长期骨髓抑制的研究进展
Long-term myelosuppression induced by irradiation
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摘要: 随着接受放疗患者生存期的延长,患者发生长期骨髓抑制的概率也大幅提高。长期骨髓抑制在临床中常被忽略,随着时间延长患者病情会逐渐加重,生活质量降低。许多长期骨髓抑制患者会形成再生障碍性贫血或者骨髓增生异常综合征,严重者可引发死亡。研究资料表明,活性氧和丝裂原活化蛋白激酶p38(P38MAPK)通路在辐射诱导长期骨髓抑制中占主要作用。笔者总结了辐射导致的长期骨髓抑制的相关研究,指出了今后的研究方向。
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关键词:
- 造血干细胞 /
- 骨髓抑制 /
- 活性氧 /
- 丝裂原活化蛋白激酶p38
Abstract: The incidence of long-term myelosuppression increased with the increasing numbers of cancer patients treated with radiation, Because long-term myelosuppression can deteriorate over time and be overlooked in clinic, the survival quality of cancer survivors are affected. Many of them may develop hypoplastic anemia or myelodysplastic syndrome, even death. The role of reactive oxygen species and p38 MAPK in regulating long-term myelosuppression induced by irradiation has been proved in the recent years. In this review, the advancement of long-term myelosuppression induced by irradiation and the further works need to be done are summarized. -
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