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Polo-like kinase 2: A new exploitable target to undermine mutant p53-dependent chemoresistance

机译:马球样激酶2:破坏突变p53依赖的化学耐药性的新的可利用的目标。

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摘要

During the last decade, the role of p53 point mutants as determinants of tumor aggressiveness was conclusively demonstrated.' Based on a large body of evidence, a more complete picture of the consequences of p53 mutation in human cancer is emerging, where a single missense mutation transforms one of the most efficient tumor suppressor pathways into a powerful network promoting tumor progression, indeed, these mutant p53 proteins are devoid of oncosuppressive abilities; on the contrary, they acquire novel oncogenic properties supporting several tumorigenic processes like cell proliferation, death resistance, genomic instability, angiogenesis and metastasis formation.
机译:在过去的十年中,p53点突变体作为肿瘤侵袭性决定因素的作用得到了最终证明。基于大量证据,正在出现关于p53突变对人类癌症后果的更完整描述,其中单个错义突变将最有效的抑癌途径之一转化为促进肿瘤进展的强大网络,实际上,这些突变p53蛋白缺乏抑癌能力;相反,它们具有新颖的致癌特性,可支持多种致瘤过程,如细胞增殖,死亡抵抗,基因组不稳定,血管生成和转移形成。

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