Targeting DNA repair pathway in cancer: Mechanisms and clinical application

被引:90
作者
Wang, Manni [1 ]
Chen, Siyuan [1 ]
Ao, Danyi [1 ]
机构
[1] Sichuan Univ, West China Hosp, Dept Biotherapy, Canc Ctr, 37 Guoxue Alley, Chengdu 610041, Sichuan, Peoples R China
来源
MEDCOMM | 2021年 / 2卷 / 04期
关键词
cancer; combination therapy; DNA damage response; PARP; DEPENDENT PROTEIN-KINASE; BASE-EXCISION-REPAIR; CELL LUNG-CANCER; POLY(ADP-RIBOSE) POLYMERASE INHIBITOR; REPLICATION FORK STABILITY; RESISTANT PROSTATE-CANCER; SMALL-MOLECULE INHIBITION; RELAPSED OVARIAN-CANCER; FANCONI-ANEMIA PATHWAY; DOUBLE-STRAND BREAKS;
D O I
10.1002/mco2.103
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
100103 [病原生物学]; 100218 [急诊医学];
摘要
Over the last decades, the growing understanding on DNA damage response (DDR) pathways has broadened the therapeutic landscape in oncology. It is becoming increasingly clear that the genomic instability of cells resulted from deficient DNA damage response contributes to the occurrence of cancer. One the other hand, these defects could also be exploited as a therapeutic opportunity, which is preferentially more deleterious in tumor cells than in normal cells. An expanding repertoire of DDR-targeting agents has rapidly expanded to inhibitors of multiple members involved in DDR pathways, including PARP, ATM, ATR, CHK1, WEE1, and DNA-PK. In this review, we sought to summarize the complex network of DNA repair machinery in cancer cells and discuss the underlying mechanism for the application of DDR inhibitors in cancer. With the past preclinical evidence and ongoing clinical trials, we also provide an overview of the history and current landscape of DDR inhibitors in cancer treatment, with special focus on the combination of DDR-targeted therapies with other cancer treatment strategies.
引用
收藏
页码:654 / 691
页数:38
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