Alterations in chromosome structure and variations in the inherent radiation sensitivity of human cells
Alterations in chromosome structure and variations in the inherent radiation sensitivity of human cells
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DOI：
10.2307/3579692
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发表时间：
1998-04-01
影响因子：
3.4
通讯作者：
Schwartz, JL
中科院分区：
文献类型：
--
作者：
Schwartz, JL
肿瘤细胞及其周围正常组织的固有放射敏感性的变化在肿瘤对放射治疗的反应中起重要作用。体外研究表明，不同组织之间和特定组织学内辐射敏感性的变化反映了染色体断裂重新连接的速率和保真度的差异。放射敏感性细胞系的细胞与更耐药的细胞系的细胞相比，重新连接断裂更慢且保真度更低。辐射敏感性的差异也与染色体结构的变化有关，如通过基于核苷酸的测定所检测到的。提出一个模型，表明辐射敏感性的细胞系是其转录结构，其活跃的转录区域的数量和基因组位置的反映。此外，有人提出，在基因组的转录活性区域或附近诱导的染色体断裂优先重新连接，并且比在基因组的其他区域诱导的断裂具有更大的保真度。(C)1998年，辐射研究会。
Variations in the inherent radiosensitivity of both tumor cells and the normal tissues that surround them play an important role in tumor response to radiation therapy. In vitro studies suggest that variations in radiation sensitivity both between different tissues and within a specific histology are a reflection of differences in the rate and fidelity of rejoining of chromosome breaks. Cells of radiosensitive cell lines rejoin breaks more slowly and with less fidelity than those of more resistant cell lines. Differences in radiation sensitivity are also associated with variations in chromosome structure as detected by nucleoid-based assays. A model is presented to suggest that the radiation sensitivity of a cell line is a reflection of its transcriptional architecture, the number and genomic location of its actively transcribing regions. Also, it is proposed that chromosome breaks induced at or near transcriptionally active regions of the genome are rejoined preferentially and with greater fidelity than breaks induced at other regions of the genome. (C) 1998 by Radiation Research Society.