【摘要】 共济失调毛细血管扩张突变基因和Rad3相关蛋白激酶是DNA修复的关键激酶，对基因组稳定以及肿瘤的发生、发展和治疗都至关重要。抑制共济失调毛细血管扩张突变基因和Rad3相关蛋白激酶可触发细胞周期阻滞，从而抑制由共济失调毛细血管扩张突变基因和Rad3相关蛋白激酶介导的修复途径，高效杀死肿瘤细胞。因此开发共济失调毛细血管扩张突变基因和Rad3相关蛋白激酶抑制剂是治疗具有DNA修复缺陷癌症的热点之一。本文主要综述了共济失调毛细血管扩张突变基因和Rad3相关蛋白激酶与DNA突变所致癌症的关联，并重点介绍了小分子共济失调毛细血管扩张突变基因和Rad3相关蛋白激酶抑制剂的研究进展，为后续基于共济失调毛细血管扩张突变基因和Rad3相关蛋白激酶的抗肿瘤药物研究提供了有益指导。更多还原

【Abstract】 Ataxia telangiectasia mutated genes and RAD3-associated protein kinase(ATR) are key kinases for DNA repair.Both of them are critical for genome stabilization as well as for tumor initiation, development, and treatment.The inhibition of ATR can trigger cell cycle arrest, thereby inhibiting the ATR-mediated repair pathway and efficiently killing tumor cells.Therefore, the development of ATR inhibitors is one of the hot spots in the treatment of cancer with DNA repair defects.This article mainly reviews the relationship between ATR and cancer caused by DNA mutation, and focuses on ATR inhibitors, which provides useful guidance for the subsequent study of tumor inhibitors.更多还原