Beyond Kinases: Targeting Replication Stress Proteins in Cancer Therapy.
Abstract
DNA replication stress describes a state of impaired replication fork progress that triggers a cellular stress response to maintain genome stability and complete DNA synthesis. Replication stress is a common state that must be tolerated in many cancers. One promising therapeutic approach is targeting replication stress response factors such as the ataxia telangiectasia and rad 3-related kinase (ATR) or checkpoint kinase 1 (CHK1) kinases that some cancers depend upon to survive endogenous replication stress. However, research revealing the complexity of the replication stress response suggests new genetic interactions and candidate therapeutic targets. Many of these candidates regulate DNA transactions around reversed replication forks, including helicases, nucleases and alternative polymerases that promote fork stability and restart. Here we review emerging strategies to exploit replication stress for cancer therapy.
References
Citations
Related Concepts
Related Feeds
Ataxia telangiectasia
Ataxia telangiectasia is a rare neurodegenerative diseases caused by defects in the ATM gene, which is involved in DNA damage recognition and repair pathways. Here is the latest research on this autosomal recessive disease.
Ataxia telangiectasia (MDS)
Ataxia telangiectasia is a rare neurodegenerative diseases caused by defects in the ATM gene, which is involved in DNA damage recognition and repair pathways. Here is the latest research on this autosomal recessive disease.