1.Inflammation-associated genomic instability in cancer | Khian Hong Pua，Chen Li Chew，David Philip Lane，Vinay Tergaonkar

Inflammation serves as a protective stimulus against foreign pathogens, but if left unchecked, it has the potential to promote carcinogenesis. In this review, Vinay Tergaonkar and colleagues outline three pathways of inflammation and highlight how chronic inflammation might cause genomic instability. The researchers explain two broad principles that govern therapeutic approaches to chronic inflammation. They clarify the consequences of chronic inflammation on genomic instability and provide essential insight as to how effective therapies might be designed based on this axis. Drs. Khian Hong Pua and Chen Li Chew are co-first authors of this review. Correspondence should be directed to Prof. Vinay Tergaonkar at the Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore.

炎症是人体抵御外来病原体必要的保护措施，但时间过长会引起慢性炎症，进而成为诱发癌变的潜在因素。本文系统地介绍了炎症的三大通路，揭示炎症导致基因不稳定的机制，同时阐述了治疗慢性炎症两个主流的解决方案，为更好的理解炎症，以及治疗慢性炎症，提供参考。

文章的第一 (共同) 作者是Khian Hong Pua和Chen Li Chew博士，通讯作者为Vinay Tergaonkar教授，来自新加坡分子细胞生物研究所，新加坡国立大学。

Vinay Tergaonkar教授  

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2.DNA double-strand break repair pathway choice: the fork in the road| Jinhua Han, Jun Huang

DNA double-strand breaks (DSBs) are a common type of DNA lesion. If unrepaired or misrepaired, DSBs can lead to genomic instability and even tumorigenesis. DSBs can be repaired by several mechanisms, depending on the type of damage. In this review, Jinhua Han and Jun Huang explain how cells choose the most appropriate DSB repair pathway upon detecting DNA damage, and outline the underlying mechanisms regulating this choice. Correspondence should be directed to professor Jun Huang at the Life Sciences Institute, Zhejiang University, China.

DNA 双链断裂（DSBs)是一种常见的DNA损伤，人体每天发生的DSBs高达数百次，如不对其进行修复或修复不当，将会导致基因的不稳定甚至发生癌变。细胞对DSBs的修复有各种不同的方式，本文对其进行详细的讲解，并揭示影响细胞做出修复选择的因素，以便我们更深刻地认识DSBs修复，为治疗HR缺陷的药物开发提供技术指导。

本文的通讯作者是黄俊教授，第一作者是韩金花博士, 来自浙江大学。

黄俊教授 

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3.Regulation of DNA damage-induced ATM activation by histone modifications | Zhiming Li, Yongcan Chen, Ming Tang, Yinglu Li, Wei-Guo Zhu

When cells repair DNA double-strand breaks (DSBs), post-translational modifications on Ataxia-telangiectasia mutated (ATM) activate ATM function, which then initiates a program of DNA damage repair. In this review, Wei-Guo Zhu and colleagues detail the histone modifications that regulate ATM activation and how they mediate the DNA damage response. Dr. Zhiming Li is the first author of this review. Correspondence should be directed to professor Wei-Guo Zhu at the School of Medicine, Shenzhen University, China.  

DNA 双链断裂（DSBs)修复过程中，细胞通过转录后修饰激活Ataxia-telangiectasia mutated (ATM)，进而引发DNA损伤修复过程。在这篇文章中，作者详细介绍了各种不同的组蛋白修饰，并揭示其在DNA损伤过程中如何调控ATM激活, 修复DNA损伤，让我们更加深刻地理解ATM激酶在DNA损伤修复过程中的重要作用，也为针对该靶点的药物设计，提供更多的思路。

李治明博士为本文的第一作者，通讯作者为朱卫国教授，来自深圳大学医学部。

朱卫国教授 

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4.Post-translational modifications of nuclear sirtuins| Kaiqiang Zhao, Zhongjun Zhou

Sirtuins constitute a protein family of NAD+ dependent deacetylases. Among them, SIRT1, SIRT6 and SIRT7 are localized to the cell nucleus. In this review, Kaiqiang Zhao and Zhongjun Zhou describe the various post-translational modifications that can occur on these nuclear sirtuins and explain how these modifications regulate sirtuin function. Improving our understanding of nuclear sirtuin function might help guide the development of new therapies for SIRT-associated diseases. Correspondence should be directed to Professor Zhongjun Zhou at the School of Biomedical Sciences, LKS Faculty of Medicine, The University of Hong Kong.

SIRT家族蛋白是一类依赖NAD+的去乙酰化酶，其中 SIRT1, SIRT6 和 SIRT7在哺乳动物中主要分布于细胞核，在应对环境压力，转录翻译，保持基因稳定，细胞衰老等方面发挥重要作用。本文详细介绍了细胞核SIRT蛋白的各种翻译后修饰，以及其对应的功能影响，对我们进一步了解SIRT蛋白及其调控和功能，提供参考。

文章的作者是Kaiqiang Zhao博士和周中军教授，来自香港大学医学院。

周中军教授 

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