细胞毒化合物预处理增敏 p53 缺陷型肺癌细胞的放射敏感性。
Radiosensitization of p53-deficient lung cancer cells by pre-treatment with cytostatic compounds.
机构信息
Biological and Molecular Imaging, OncoRay -- National Center for Radiation Research in Oncology, Carl Gustav Carus Medical Faculty, Dresden University of Technology, Dresden, Germany.
出版信息
Anticancer Res. 2012 Apr;32(4):1239-43.
BACKGROUND/AIM: This study specifies a strategy to improve radiotherapy by partial synchronization of p53-deficient cancer cells (FaDu and H1299) in mitosis using taxol, with protecting p53 wild-type cells (A549) by the prior administration of cytostatic compounds. Cytotoxic and cytostatic effects of ionizing radiation, cisplatin, doxorubicin and taxol, administrated alone or in combination were investigated in vitro by flow cytometry.
RESULTS
A protective effect of doxorubicin but not cisplatin was found after administration of triple sequence with ionizing radiation and taxol. It was found that preliminary administration of doxorubicin induced growth arrest and protected A549 cells from the taxol/radiation treatment, while simultaneously killing FaDu and H1299 cells.
CONCLUSION
The proposed therapeutic strategy allows protection of p53 wild-type cells and selectively increases radiosensitivity of p53-deficient cancer cells.
背景/目的：本研究采用紫杉醇使 p53 缺陷型癌细胞（FaDu 和 H1299）部分同步有丝分裂，从而制定出一种改进放射疗法的策略，并用细胞抑制剂预先保护 p53 野生型细胞（A549）。采用流式细胞术，体外研究了电离辐射、顺铂、阿霉素和紫杉醇单独或联合应用的细胞毒性和细胞抑制作用。
结果
在给予电离辐射和紫杉醇的三联序列后，发现阿霉素具有保护作用，但顺铂没有。结果发现，预先给予阿霉素可诱导细胞生长停滞，并使 A549 细胞免受紫杉醇/辐射治疗的影响，同时杀死 FaDu 和 H1299 细胞。
结论
所提出的治疗策略允许保护 p53 野生型细胞，并选择性地增加 p53 缺陷型癌细胞的放射敏感性。
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