辐射导致长期骨髓抑制的研究进展  

Long-term myelosuppression induced by irradiation

作　　者：李德冠[1] 樊赛军[1] 孟爱民[1] 

机构地区：[1]中国医学科学院放射医学研究所、天津市放射医学和分子核医学重点实验室,天津300192

出　　处：《国际放射医学核医学杂志》2015年第4期324-327,共4页International Journal of Radiation Medicine and Nuclear Medicine

基　　金：国家重点基础研究发展计划（2011CB964800-G）;国家自然科学基金（81372928,81102873）;天津自然科学基金（12JCQNJC09100,15JCZDJC35200）

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。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.

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 

分 类 号：R730.55[医药卫生—肿瘤]