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恶性胶质瘤化疗面临二大难题,一是肿瘤化疗药不敏感和耐药,二是化疗的有效剂量同中毒剂量常很接近.副作用大,在杀伤瘤细胞的同时也杀伤正常细胞.人们在寻找特异性杀伤肿瘤药物同时,还试图利用基因工程技术改变肿瘤细胞的药物敏感性,近来的研究发现放疗和化疗可以引起肿瘤细胞凋亡,而是否发生凋亡同肿瘤 p~53基因的状态有关.本实验证实野生型p~53基因(Wt-p~53)能增强9L胶质肉瘤细胞化疗敏感性,钙通道阻滞剂尼莫地平有协同作用.钙通道抑制剂的作用机制还不完全清楚,但有一些细胞的凋亡并无Ca~(2+)的活动.目前认为凋亡的DNA lader是由于细胞内Ca~(2+)、Mg~(2+)依赖性核酸内切酶把DNA切成180-200bp不同倍数的核酸片段形成的.该酶需要 Ca~(2+)激活.肿瘤细胞凋亡是否由Ca~(2+)通道引起,取决于细胞是否存在Ca~(2+)依赖性核
Chemotherapy of malignant glioma faces two major problems, one is insensitive to chemotherapy and drug resistance of the tumor, and second, the effective dose of chemotherapy is often very close with the dose. Side effects, kill the tumor cells but also kill normal cells. At the same time, it is trying to change the drug sensitivity of tumor cells by using genetic engineering techniques. Recently, we found that radiotherapy and chemotherapy can cause tumor cell apoptosis, but whether apoptosis occurs is related to the state of tumor gene p ~ 53 This experiment confirmed that the wild-type p53 gene (Wt-p53) can enhance the chemosensitivity of 9L gliosarcoma cells, and the calcium channel blocker Nimodipine has a synergistic effect.The mechanism of calcium channel inhibitor is not complete However, some of the cells have no Ca 2+ activity and apoptosis is thought to be due to intracellular Ca 2+, Mg 2+ -dependent endonucleases The DNA is cut into different multiples of 180-200bp to form a nucleic acid fragment that requires Ca2 + activation. Whether tumor cell apoptosis is caused by Ca2 + channels depends on the presence or absence of Ca2 + +) Dependent kernels