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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Influence of p53 Status on the Effects of Boron Neutron Capture Therapy in Glioblastoma
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Influence of p53 Status on the Effects of Boron Neutron Capture Therapy in Glioblastoma

机译：p53的状态对胶质母细胞瘤中子捕获硼治疗效果的影响

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Background/Aim: The tumor suppressor gene p53 is mutated in glioblastoma. We studied the relationship between the p53 gene and the biological effects of boron neutron capture therapy (BNCT). Materials and Methods: The human glioblastoma cells; A172, expressing wild-type p53, and T98G, with mutant p53, were irradiated by the Kyoto University Research Reactor (KUR). The biological effects after neutron irradiation were evaluated by the cell killing effect, 53BP1 foci assay and apoptosis induction. Results: The survival-fraction data revealed that A172 was more radiosensitive than T98G, but the difference was reduced when boronophenylalanine (BPA) was present. Both cell lines exhibited similar numbers of foci, suggesting that the initial levels of DNA damage did not depend on p53 function. Detection of apoptosis revealed a lower rate of apoptosis in the T98G. Conclusion: BNCT causes cell death in glioblastoma cells, regardless of p53 mutation status. In T98G cells, cell killing and apoptosis occurred effectively following BNCT.
机译：背景/目的：胶质母细胞瘤中的抑癌基因p53发生了突变。我们研究了p53基因与硼中子捕获疗法（BNCT）的生物学效应之间的关系。材料与方法：人胶质母细胞瘤细胞;京都大学研究堆（KUR）辐射了表达野生型p53的A172和具有突变型p53的T98G。通过细胞杀伤作用，53BP1病灶测定和凋亡诱导评价中子辐照后的生物学作用。结果：生存分数数据显示，A172比T98G对放射线敏感，但当存在硼苯丙氨酸（BPA）时，差异有所减小。两种细胞系均显示出相似数量的病灶，表明DNA损伤的初始水平不依赖于p53功能。检测细胞凋亡显示出T98G中较低的细胞凋亡率。结论：无论p53突变状态如何，BNCT均可导致胶质母细胞瘤细胞死亡。在T98G细胞中，BNCT后有效地发生了细胞杀伤和凋亡。

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