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Tumor resistance to specific lysis: a major hurdle for successful immunotherapy of cancer.

机译:肿瘤对特异性裂解的抵抗力:成功进行癌症免疫治疗的主要障碍。

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Research over the past decade in tumor immunology has shown that immune reactivity to tumor antigens can decrease tumor growth in experimental models. These observations have been translated into clinical studies involving both passive and active forms of immunotherapy. Immunotherapy, an alternative treatment for cancer, is confronted to a major hurdle: tumor escape of specific lysis. Cancer antigen-specific cytotoxic T lymphocytes (CTL) are the major effectors used in immunotherapy against cancer cells. However, large established tumors are usually not fully controlled by CTL. These effector cells could indeed have a dual activity, which allow cancer cells to escape destruction. In this review, we will focus on the essential role of the p53 tumor suppressor gene in the dynamic regulation of tumor cell death induced by cytotoxic T lymphocytes and the involving of structural changes of cytoskeleton in the acquisition of tumor resistance.
机译:过去十年中肿瘤免疫学的研究表明,对肿瘤抗原的免疫反应可降低实验模型中的肿瘤生长。这些观察结果已转化为涉及被动和主动免疫疗法形式的临床研究。免疫疗法是癌症的另一种治疗方法,它面临着一个主要障碍:特异性裂解的肿瘤逃逸。癌症抗原特异性细胞毒性T淋巴细胞(CTL)是用于针对癌细胞的免疫疗法的主要效应物。但是,大型已确立的肿瘤通常不能完全由CTL控制。这些效应细胞确实可以具有双重活性,使癌细胞能够逃脱破坏。在这篇综述中,我们将重点研究p53抑癌基因在动态调节由细胞毒性T淋巴细胞诱导的肿瘤细胞死亡中的重要作用,以及在获得抗药性中涉及细胞骨架的结构变化。

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