Radiation sensitivities of 31 human oesophageal squamous cell carcinoma cell lines
Radiation sensitivities of 31 human oesophageal squamous cell carcinoma cell lines
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DOI：
10.1111/j.0959-9673.2005.00431.x
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发表时间：
2005-08-01
影响因子：
3
通讯作者：
Imai, T
中科院分区：
文献类型：
--
作者：
Ban, S;Michikawa, Y;Imai, T
本研究旨在用集落形成实验测定31株人食管鳞癌细胞系的放射敏感性。31个细胞系的放射敏感性存在较大差异。如此大的变异可能部分解释了这种癌症放射治疗效果不佳的原因。一个细胞系（KYSE 190）表现出不寻常的放射敏感性。这些细胞中的共济失调毛细血管扩张突变（ATM）基因有5个错义突变，ATM蛋白被截短或降解。在照射的KYSE 190细胞中不能磷酸化Chk2表明这些细胞中的ATM蛋白已经失去了其功能。ATM蛋白功能失调可能是KYSE 190细胞放射敏感性异常的主要原因。由于这些细胞的供体未被诊断为共济失调毛细血管扩张症，ATM基因突变可能发生在癌症的发生和发展过程中。非遗传性疾病患者发生的放射敏感性肿瘤应是放射治疗的良好靶点。
The purpose of this study was to determine the radiosensitivities of 31 human oesophageal squamous cell carcinoma cell lines with a colony-formation assay. A large variation in radiosensitivity existed among 31 cell lines. Such a large variation may partly explain the poor result of radiotherapy for this cancer. One cell line (KYSE190) demonstrated an unusual radiosensitivity. Ataxia-telangiectasia-mutated (ATM) gene in these cells had five missense mutations, and ATM protein was truncated or degraded. Inability to phosphorylate Chk2 in the irradiated KYSE190 cells suggests that the ATM protein in these cells had lost its function. The dysfunctional ATM protein may be a main cause of unusual radiosensitivity of KYSE190 cells. Because the donor of these cells was not diagnosed with ataxia telangiectasia, mutations in ATM gene might have occurred during the initiation and progression of cancer. Radiosensitive cancer developed in non-hereditary diseased patients must be a good target for radiotherapy.