Editorial: DNA repair and nucleic acid therapeutics in cancer.

Editorial: DNA repair and nucleic acid therapeutics in cancer.
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DOI:
10.1093/narcan/zcad044
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发表时间:
2023-09
期刊:
影响因子:
5.1
通讯作者:
--
中科院分区:
其他
文献类型:
--
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文献摘要

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NAR Cancer 很高兴发表一系列文章 [ https://academic.奥普。 com/narcancer/pages/dna-repair-andnucleic-acids-therapeutics] 强调围绕“癌症中的 DNA 修复和核酸治疗”主题的靶向 DNA 修复和 DNA 损伤反应机制的突破和前景。 11 篇评论文章提供了对影响基因组稳定性和肿瘤发生的 DNA 修复机制的见解,概述了当前和未来专注于 DNA 损伤和修复机制的癌症治疗方案,并重点介绍了促进我们对 DNA 修复和 DNA 损伤反应蛋白和通路之间串扰的理解的方法。该在线合集还包含 NAR Cancer 自 2020 年成立以来已发表的超过 40 篇关于 DNA 修复和核酸治疗相关主题的标准文章的链接。人类接触危险的基因毒素是不可避免的,因为 DNA 损伤剂在我们的环境和细胞内无处不在 (1, 2)。由细胞代谢、环境来源或疾病相关细胞缺陷产生的 DNA 损伤剂和其他基因毒素会导致细胞死亡、基因突变、基因重排,在许多情况下还会导致癌症、疾病和衰老表型的发生 (3-6)。因此,基因组的维护依赖于无差错的 DNA 复制、RNA 转录和端粒稳定性。这是通过 DNA 修复和响应机制的复杂网络来实现的,该网络能够响应内源性和外源性基因毒素的 DNA 损伤。这种蛋白质机器网络参与并激活以响应多种类型的基因组损伤,被称为 DNA 损伤反应 (DDR)(7)。
NAR Cancer is pleased to publish a collection of articles [ https://academic. oup. com/narcancer/pages/dna-repair-andnucleic-acids-therapeutics] highlighting the breakthroughs and promise of targeting DNA Repair and DNA damage re-sponse mechanisms centered around the theme of ‘DNA Repair and Nucleic Acid Therapeutics in Cancer’. Eleven review articles provide insights into DNA repair mechanisms that impact genome stability and tumorigenesis, outline current and future cancer therapeutic options focused on DNA damage and repair mechanisms, and highlight methods to advance our understanding of the crosstalk among DNA repair and DNA damage response proteins and pathways. The online collection also includes links to> 40 Standard Articles on DNA repair and nucleic acids therapeutic-related topics that NAR Cancer has published since its inception in 2020.Human exposure to dangerous genotoxins is unavoidable, as DNA damaging agents are ubiquitous both in our environment and within our cells (1, 2). DNA damaging agents and other genotoxins that arise from cellular metabolism, environmental sources or disease-related cellular defects contribute to cell death, gene mutations, gene rearrangements and in many cases, the onset of cancer, disease, and aging phenotypes (3–6). Maintenance of the genome is therefore dependent on error-free DNA replication, RNA transcription and telomere stability. This is accomplished by a complex network of DNA repair and response mechanisms able to respond to DNA insults from both endogenous and exogenous genotoxins. This network of protein machines, engaged and activated in response to numerous types of genome damage, is referred to as the DNA damage response (DDR)(7).