p53 Targeting can enhance cancer therapy via radiation, heat and anti-cancer agents.

p53 Targeting can enhance cancer therapy via radiation, heat and anti-cancer agents.
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DOI:
10.2174/187152008784533017
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发表时间:
2008-05
影响因子:
2.8
通讯作者:
T. Ohnishi;A. Takahashi;Eiichiro Mori;K. Ohnishi
T. Ohnishi;A. Takahashi;Eiichiro Mori;K. Ohnishi
中科院分区:
医学4区
文献类型:
--
作者:
T. Ohnishi;A. Takahashi;Eiichiro Mori;K. Ohnishi

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近年来,人们对与癌症相关的基因进行了研究,以评估它们作为癌症治疗预测指标的可能性。其中,肿瘤抑制基因p53的基因产物被发现在癌症治疗中发挥重要作用。在细胞受到辐射、热和各种抗癌药物的癌症治疗后,p53分子诱导细胞周期阻滞、细胞凋亡和DNA修复。p53突变在人类肿瘤中被观察到的频率很高,并且存在于大约一半的人类恶性肿瘤中。在含有野生型p53的细胞中观察到对辐射、热和抗癌药物的敏感性,而在含有突变型p53的细胞中则没有。本文综述了暴露于以p53为靶点的癌症治疗后p53信号通路的激活;这些治疗方法包括化学伴侣、p53基因、p53-c末端肽和p53靶向药物,这些药物可以增强p53中枢信号转导通路。
In recent years, genes associated with cancer have been studied to assess their possible use as predictive indicators for cancer therapies. Among these, the gene product of the tumor suppressor gene p53 was found to play an important role in cancer therapy. The p53 molecule induces cell-cycle arrest, apoptosis and DNA repair after cells are subjected to cancer therapies involving radiation, heat and various anti-cancer agents. Mutations in p53 are observed at a high frequency in human tumors, and are present in about half of all malignant tumors in humans. Sensitization to radiation, heat and anti-cancer agents was observed in cells containing wild type p53, but not in cells containing mutated p53. This review discusses p53 activation of signaling pathways after exposure to cancer therapies which target p53; such therapies include chemical chaperones, the p53 gene, p53-C terminal peptides, and p53-targeting agents which enhance p53-central signal transduction pathways.