联合治疗与靶向抗癌耐药性
Polytherapy and Targeted Cancer Drug Resistance.
作者信息
Chatterjee Nilanjana, Bivona Trever G
机构信息
Department of Medicine, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA; Department of Cellular and Molecular Pharmacology, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA; Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA.
Department of Medicine, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA; Department of Cellular and Molecular Pharmacology, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA; Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA.
出版信息
Trends Cancer. 2019 Mar;5(3):170-182. doi: 10.1016/j.trecan.2019.02.003. Epub 2019 Feb 26.
A current challenge in cancer treatment is drug resistance. Even the most effective therapies often fail to produce a complete and durable tumor response and ultimately give rise to therapy resistance and tumor relapse. However, how resistance arises in cancer remains incompletely understood. While drug resistance in cancer is thought to be driven by irreversible genetic mutations, emerging evidence also implicates reversible proteomic and epigenetic mechanisms in the development of drug resistance. Tumor microenvironment-mediated mechanisms and tumor heterogeneity can significantly contribute to cancer treatment resistance. Here, we discuss the diverse and dynamic strategies that cancers use to evade drug response, the promise of upfront combination and intermittent therapies and therapy switching in forestalling resistance, and epigenetic reprogramming to combat resistance.
癌症治疗当前面临的一个挑战是耐药性。即使是最有效的疗法也常常无法产生完全且持久的肿瘤反应，最终导致治疗耐药和肿瘤复发。然而，癌症中耐药性是如何产生的仍未完全明确。虽然癌症中的耐药性被认为是由不可逆的基因突变驱动的，但新出现的证据也表明可逆的蛋白质组学和表观遗传学机制在耐药性的发展中起作用。肿瘤微环境介导的机制和肿瘤异质性可显著导致癌症治疗耐药。在此，我们讨论癌症用于逃避药物反应的多样且动态的策略、前期联合治疗和间歇治疗以及治疗转换在预防耐药方面的前景，以及通过表观遗传重编程来对抗耐药性。
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