1. PRMT1 and PRMT5: on the road of homologous recombination and non-homologous end joining | Shasha Yin, Liu Liu & Wenjian Gan

Homologous recombination (HR) and non homologous end joining (NHEJ) constitute the two main repair pathways used by cells to respond to DNA double strand breaks (DSBs). Protein arginine methyltransferases (PRMTs) are a key family of regulatory factors that regulate DNA damage repair. In this review, Professor Wenjian Gan and colleagues from South Carolina Medical University (USA) summarize the regulatory roles of PRMT1 and PRMT5 specifically. They discuss their contribution to DSB repair pathway choice and their regulation of HR and NHEJ, and how they might be targeted in cancer therapy.

Fig.1 The process and major components of HR and NHEJ.

同源重组（HR）和非同源末端连接（NHEJ）是细胞应对DNA双链断裂的两种主要修复途径。蛋白质精氨酸甲酯转移酶（PRMT）是调控DNA损伤修复关键的调节因子。在这篇综述中，来自美国南卡罗来纳医科大学的甘文剑教授团队总结了目前PRMT1和PRMT5在DSB修复途径选择中的调控作用，帮助我们更好地了解该领域的最新进展。

甘文剑教授

全文链接：https://link.springer.com/article/10.1007/s42764-022-00095-w

2. DNA damage repair and cancer immunotherapy | Zhiyuan Xiang, Hao Liu & Ying Hu  

DNA damage repair (DDR) is an important mechanism that has evolved to allow cells to cope with various endogenous and exogenous stresses. Any impairment to DDR pathways can lead to an accumulation of DNA damage and subsequent genomic instability. In this review, Professor Ying Hu and colleagues from Harbin Institute of Technology (China) outline the mechanisms by which DNA damage can occur, the DDR pathways that can be elicited to counteract damage, and the known associations between altered DDR pathways and cancer risk. Finally, the authors speculate on how a DDR deficiency is associated with cancer immunity, and how this information might be leveraged to develop new cancer therapeutics.

Fig.2 DNA damage repair and cancer immunotherapy

DNA损伤修复（DDR）是细胞应对多种内源性外源性应激的重要手段，DDR受损可导致DNA损伤和基因组不稳定的积累，最终导致癌症的发生。在这篇综述中，哈尔滨工业大学的胡颖教授和同事概述了DNA损伤的机制，抵消它们的DDR途径，并总结了DDR途径改变与癌症之间的联系。

胡颖教授

全文链接：https://link.springer.com/article/10.1007/s42764-023-00098-1

3. Clonal evolution in leukemia: preleukemia, evolutionary models, and clinical implications| Xu-Dong He, Meng-Fang Xia, Ji-Yuan Teng, Bin-Bing S. Zhou & Qian-Fei Wang

Leukemia is a polyclonal and progressive disease with drastic intra-clone heterogeneity. In this review, Bin-Bing S. Zhou from Shanghai Children’s Medical Center, Shanghai Jiao Tong University, Qian-Fei Wang from Beijing Institute of Genomics, CAS, and colleagues summarize the current understanding of how genetic lesions define distinct clonal architectures. They highlight two classical evolutionary models of clonal architectures and then speculate on their relevant prognostic implications. They also discuss the common recurrent patterns of clonal evolution that occur in patients undergoing chemotherapy and targeted therapy. Improving our knowledge in this area is expected to drive forward the development of new strategies to prevent or overcome drug resistance and relapse.

Fig. 3 Clonal evolution in leukemia: preleukemia, evolutionary models, and clinical implications.

白血病是一种多克隆和进行性疾病，具有严重的克隆内异质性。来自上海交通大学上海儿童医学中心的周斌兵教授和中科院北京基因组研究所的王前飞教授团队总结了目前对遗传病变如何定义不同克隆结构的理解。进一步强调了两个经典的进化模型及其相关的预后影响, 并讨论了化疗和靶向治疗下克隆进化的复发模式。

王前飞教授

周斌兵教授

全文链接： https://link.springer.com/article/10.1007/s42764-023-00104-6

4. Major genomic mutations driving hepatocellular carcinoma | Ran Chen, Moubin Lin & Daming Gao

Hepatocellular carcinoma (HCC) is a subtype of a highly malignant carcinoma that occurs in the liver. By improving our understanding of the mechanisms underlying HCC tumorigenesis we stand to improve the clinical treatment options for affected patients. Data suggest that HCC tumorigenesis and progression are driven by various genomic mutations and alterations. In this review, Daming Gao and colleagues at the CAS Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai (China) provide an overview of driver mutations in different signaling pathways that dominate HCC tumorigenesis, and the vital molecular events involved in HCC initiation. They also summarize the different treatment modalities that can be applied depending on the corresponding mutation events. The authors hope that expanding our understanding of the inherent characteristics of HCC will open up new avenues for new clinical treatment options in the future.  

Fig. 4  Major genomic mutations driving hepatocellular carcinoma.

肝细胞癌（HCC）是发生在肝脏中的高度恶性癌症的一种亚型，迫切需要更好地了解HCC肿瘤发生的机制和更好的临床治疗方案。一些证据表明，HCC的肿瘤发生和发展是由各种基因组突变和改变驱动的。在这篇综述中，来自中科院上海分子细胞科学卓越中心的高大明团队概述了主导HCC肿瘤发生的不同信号通路中的驱动突变，以及HCC发生中的重要分子事件，以及总结了可用于治疗具有相应突变事件的HCC患者不同的药物或工具。这些发现可能扩大我们对HCC固有特征的理解，为未来HCC的临床治疗提供参考。

高大明研究员

全文链接：https://link.springer.com/article/10.1007/s42764-023-00103-7