Publication details
Synthetic Lethality, A therapeutic approach
| Authors | |
|---|---|
| Year of publication | 2014 |
| Type | Appeared in Conference without Proceedings |
| MU Faculty or unit | |
| Citation | |
| Description | Complex networks of redundant surveillance mechanisms, namely evolutionarily conserved DNA damage response (DDR) and checkpoints, maintain genomic integrity following various genomic insults. Exploring synthetic lethal interactions between DNA repair pathways have wide appliance to the treatment of many types of malignancies. One of the key players in genome surveillance pathways is a protein kinase, CHK1. DNA damage and replication stress supposedly induces activation of CHK1, which then transduces the checkpoint signal and aids cell cycle arrest allowing time for DNA repair. Hence, CHK1 represents druggable molecular target for inhibition following replication stress induced by chemotherapeutic agents. Such synthetic lethal interaction leads to enhanced sensitivity of cancer cells with additional burden of damaged DNA, without cytotoxic effects to the normal cells. |