RE: Anyone read or translate Chinese15 May 2020 22:42
Best I can do on first part :- Yan Jiangdong, Wang Yinghui, Wan Yue (Chongqing University Affiliated Oncology Hospital / Chongqing Cancer Research Institute / Chongqing Cancer Hospital Oncology Radiotherapy Center, Chongqing 400030)
Key words: tumors; inhibitors; DNA damage repair; genes
Human cells produce a large number of different types of damage every day under the action of internal and external source DNA damage factors, and human cells also have a sound DNA repair mechanism to deal with these damage, restore the integrity and fidelity of DNA, so as to maintain genetic stability. There is growing evidence that DNA repair function changes during tumor occurrence, development, and treatment, and these changes are likely to be closely related to the various biological behaviors of tumors. Many carcinogens cause mutations in genes through damage to genomic DNA, and once key genes in the DNA damage response (DDR) pathway, such as BRCA1, BRCA2, BLM, FANCA, TP53, RAD51C and MSH2, mutate, can further lead to DNA repair functional defects and lead to genomic instability, which can easily increase the risk of cancer. Tumor cells carry a large number of mutant genes, DNA replication will produce a replication fork block that triggers DDR causes apoptosis, when the redox reaction-related genes are inactivated in a mutant state, oxidative stress produced by the reactive oxygen free radicals (ROS) can cause DNA oxidation damage. Therefore, we can use DNA repair inhibitors to amplify the effects of DNA replication stress and oxidative stress, to push through the limits of tumor cells' tolerance to these effects, and ultimately to produce irreversible DNA damage and lead to tumor cell death. This paper summarizes the current clinical research status of various DNA repair inhibitors, and summarizes the necessity of screening therapeutic prediction markers and the feasibility of exploring new joint treatment strategies.