Misrepair using radiosensitizer and radiosensitivity under non cycling cells

我们已经证明了AKT是否是重要的分子靶点，以控制放射抗性通过激活的AKT之间的CD 133+和CD 133-胶质瘤肿瘤细胞电离辐射治疗后比较。 当使用Mirin时，我们发现IR诱导的AKT磷酸化在CD 133+肿瘤细胞中比在CD 133-肿瘤细胞中更明显。 我们的数据表明，表达CD 133+的肿瘤细胞，干细胞的标记，诱导AKT比CD 133-细胞辐射后激活。 根据该结果，可以说CD 133+细胞在细胞放射敏感性中响应于DNA损伤具有更大的修复活化。用荧光原位杂交（FISH）技术检测X射线和重离子对正常细胞PLDR的影响。结果表明，重离子对PLDR和PLD条件下的离子交换反应相似，表明重离子对非周期性细胞和周期性细胞同样有效。

We have demonstrated whether AKT is important molecular targets to control the radioresistance through the activation of phospholitated AKT compared between CD133+ and CD133- glioma tumour cells after ionizing radiation treatment. We showed IR-induced AKT phosphorylation in CD133+ tumour cells than CD133- tumour cells when mirin was used. Our data suggested that the tumour cells expressing CD133+, a maker for the stem cell, was induced the activation of AKT more than CD133- cells after radiation. From this result, it may be said that CD133+cells have greater repair activation in response to DNA damage in cellular radiosensitivity. Confluent normal cells were exposed to X-rays and heavy ions and PLDR was studied using FISH technique. It was found that heavy ions induce similar exchanges between PLDR and PLD condition, suggesting that heavy ion therapy is as effective to non-cycling cells as cycling cells.