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首页> 外文期刊>Cell cycle >DeltaNp63alpha levels correlate with clinical tumor response to cisplatin.
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DeltaNp63alpha levels correlate with clinical tumor response to cisplatin.

机译:DeltaNp63alpha水平与临床肿瘤对顺铂的反应有关。

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摘要

After exposure to damaging agents, the p53 tumor suppressor is stabilized mediating cell cycle arrest and apoptosis. p53 family member, DeltaNp63 promotes cell proliferation and accelerates tumor growth. We previously found that the genotoxic stress agents induced a decrease of DeltaNp63alpha. We further observed that genotoxic stress mediated phosphorylation of DeltaNp63alpha targeting it into proteasome degradation. Here, we found that high DeltaNp63 protein levels in primary tumors accurately predicted response to platinum based chemotherapy and a favorable outcome in head and neck cancer patients. Our data suggest that degradation of DeltaNp63alpha is part of the cellular response to DNA damage in head and neck cancers. The findings may have implications for the rational use of DNA damaging agents in human cancer.
机译:暴露于破坏剂后,p53肿瘤抑制因子稳定下来,介导细胞周期停滞和凋亡。 p53家族成员DeltaNp63促进细胞增殖并加速肿瘤生长。我们以前发现,遗传毒性应激剂诱导了DeltaNp63alpha的减少。我们进一步观察到,遗传毒性应激介导了靶向其进入蛋白酶体降解的DeltaNp63alpha的磷酸化。在这里,我们发现原发性肿瘤中的高DeltaNp63蛋白水平准确地预测了基于铂的化学疗法的反应,并在头颈癌患者中取得了良好的疗效。我们的数据表明,DeltaNp63alpha的降解是头颈癌对DNA损伤的细胞反应的一部分。这些发现可能对在人类癌症中合理使用DNA破坏剂有影响。

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