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接受放疗患者的继发性致癌作用:关于人类、非人灵长类动物、犬类和啮齿类动物辐射诱发癌症数据的综述

Secondary carcinogenesis in patients treated with radiation: a review of data on radiation-induced cancers in human, non-human primate, canine and rodent subjects.

作者信息

Suit Herman, Goldberg Saveli, Niemierko Andrzej, Ancukiewicz Marek, Hall Eric, Goitein Michael, Wong Winifred, Paganetti Harald

机构信息

Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

出版信息

Radiat Res. 2007 Jan;167(1):12-42. doi: 10.1667/RR0527.1.

Abstract

Concern for risk of radiation-induced cancer is growing with the increasing number of cancer patients surviving long term. This study examined data on radiation transformation of mammalian cells in vitro and on the risk of an increased cancer incidence after irradiation of mice, dogs, monkeys, atomic bomb survivors, occupationally exposed persons, and patients treated with radiation. Transformation of cells lines in vitro increased linearly with dose from approximately 1 to approximately 4-5 Gy. At <0.1 Gy, transformation was not increased in all studies. Dose-response relationships for cancer incidence varied with mouse strain, gender and tissue/organ. Risk of cancer in Macaca mulatta was not raised at 0.25-2.8 Gy. From the atomic bomb survivor study, risk is accepted as increasing linearly to 2 Sv for establishing exposure standards. In irradiated patients, risk of cancer increased significantly from 1 to 45 Gy (a low to a high dose level) for stomach and pancreas, but not for bladder and rectum (1-60 Gy) or kidney (1-15 Gy). Risk for several organs/tissues increased substantially at doses far above 2 Gy. There is great heterogeneity in risk of radiation-associated cancer between species, strains of a species, and organs within a species. At present, the heterogeneity between and within patient populations of virtually every parameter considered in risk estimation results in substantial uncertainty in quantification of a general risk factor. An implication of this review is that reduced risks of secondary cancer should be achieved by any technique that achieved a dose reduction down to approximately [corrected] 0.1 Gy, i.e. dose to tissues distant from the target. The proportionate gain should be greatest for dose decrement to less than 2 Gy.

摘要

随着长期存活的癌症患者数量不断增加,对辐射诱发癌症风险的担忧也与日俱增。本研究审查了有关哺乳动物细胞体外辐射转化的数据,以及小鼠、狗、猴子、原子弹幸存者、职业受照人员和接受放射治疗患者在照射后癌症发病率增加风险的数据。体外细胞系的转化随剂量从约1 Gy线性增加至约4 - 5 Gy。在<0.1 Gy时,并非所有研究中转化都增加。癌症发病率的剂量反应关系因小鼠品系、性别和组织/器官而异。食蟹猴在0.25 - 2.8 Gy时癌症风险未升高。从原子弹幸存者研究来看,为确立照射标准,风险被认为在2 Sv以内呈线性增加。在接受照射的患者中,胃和胰腺的癌症风险在1至45 Gy(从低剂量水平到高剂量水平)显著增加,但膀胱和直肠(1 - 60 Gy)或肾脏(1 - 15 Gy)则不然。在远高于2 Gy的剂量下,多个器官/组织的风险大幅增加。物种之间、同一物种的品系之间以及同一物种内的器官之间,辐射相关癌症风险存在很大异质性。目前,风险评估中考虑的几乎每个参数在患者群体之间和群体内部都存在异质性,这导致在量化一般风险因素时存在很大不确定性。本综述的一个启示是,任何能将剂量降低至约[校正后]0.1 Gy(即远离靶区组织的剂量)的技术都应能降低继发性癌症风险。剂量降低至小于2 Gy时,相应的获益应该最大。

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