ICRP Publication 131: Stem cell biology with respect to carcinogenesis aspects of radiological protection
ICRP Publication 131: Stem cell biology with respect to carcinogenesis aspects of radiological protection
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DOI：
10.1177/0146645315621849
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发表时间：
2016-06-01
影响因子：
--
通讯作者：
Yamashita, S.
中科院分区：
文献类型：
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作者：
Hendry, J. H.;Niwa, O.;Yamashita, S.
从造血组织、乳腺、甲状腺、消化道、肺、皮肤和骨骼等方面综述了干细胞的特性、维持和更新、随年龄的进化、在壁龛中的位置以及对急性和长期暴露的辐射敏感性的最新知识。致癌目标细胞的特性继续指向更原始且基本静止的干细胞群体(能够积累导致恶性肿瘤所需的长期突变序列)，在少数组织中，指向子代祖细胞。有几个生物学过程可以帮助保护干细胞免受突变积累的影响：(1)准确的DNA修复；(2)快速诱导受损干细胞的死亡；(3)在某些组织的分裂过程中保留完整的亲本链，以便突变传递给子代分化细胞；(4)干细胞竞争，即未受损的干细胞竞争受损的干细胞，以便在关键的利基中驻留。DNA修复主要在照射后几天内进行，而干细胞复制和竞争需要数周或数月的时间，具体取决于组织类型。这一基础被用来为防护问题提供生物学见解，包括线性-非阈值和相对风险模型、组织间癌症风险的差异、剂量率效应以及按年龄和达到年龄划分的辐射致癌风险的变化。
Current knowledge of stem cell characteristics, maintenance and renewal, evolution with age, location in niches', and radiosensitivity to acute and protracted exposures is reviewed regarding haematopoietic tissue, mammary gland, thyroid, digestive tract, lung, skin, and bone. The identity of the target cells for carcinogenesis continues to point to the more primitive and mostly quiescent stem cell population (able to accumulate the protracted sequence of mutations necessary to result in malignancy), and, in a few tissues, to daughter progenitor cells. Several biological processes could contribute to the protection of stem cells from mutation accumulation: (1) accurate DNA repair; (2) rapid induced death of injured stem cells; (3) retention of the intact parental strand during divisions in some tissues so that mutations are passed to the daughter differentiating cells; and (4) stem cell competition, whereby undamaged stem cells outcompete damaged stem cells for residence in the vital niche. DNA repair mainly operates within a few days of irradiation, while stem cell replications and competition require weeks or many months depending on the tissue type. This foundation is used to provide a biological insight to protection issues including the linear-non-threshold and relative risk models, differences in cancer risk between tissues, dose-rate effects, and changes in the risk of radiation carcinogenesis by age at exposure and attained age.