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How Darwinian models inform therapeutic failure initiated by clonal heterogeneity in cancer medicine

机译:达尔文模型如何告知癌症医学中克隆异质性引发的治疗失败

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摘要

Carcinogenesis is an evolutionary process that establishes the ‘hallmarks of cancer' by natural selection of cell clones that have acquired advantageous heritable characteristics. Evolutionary adaptation has also been proposed as a mechanism that promotes drug resistance during systemic cancer therapy. This review summarises the evidence for the evolution of resistance to cytotoxic and targeted anti-cancer drugs according to Darwinian models and highlights the roles of genomic instability and high intra-tumour genetic heterogeneity as major accelerators of this evolutionary process. Clinical implications and strategies that may prevent the evolution of resistance or target the origins of genetic heterogeneity are discussed. New technologies to measure intra-tumour heterogeneity and translational research on serial biopsies of cancer lesions during and after therapeutic intervention are identified as key areas to further the understanding of determinants and mechanisms of the evolution of drug resistance.
机译:致癌作用是一个进化过程,通过自然选择获得有利遗传特性的细胞克隆来建立“癌症标志”。还提出了进化适应作为在全身性癌症治疗过程中提高耐药性的机制。这篇综述总结了根据达尔文模型对细胞毒性和靶向抗癌药物耐药性演变的证据,并强调了基因组不稳定性和高肿瘤内遗传异质性在这一进化过程中的主要促进作用。讨论了可能阻止耐药性进化或靶向遗传异质性起源的临床意义和策略。在治疗干预期间和之后,用于测量肿瘤内异质性的新技术和对癌症病变系列活检的转化研究被确定为进一步了解决定因素和耐药性进化机制的关键领域。

著录项

  • 作者

    Gerlinger, M; Swanton, C;

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  • 年度 2010
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  • 原文格式 PDF
  • 正文语种 {"code":"en","name":"English","id":9}
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