SAMADDER, Pounami. Exploring synthetic lethal interaction between Checkpoint Kinase 1(CHK1) and DNA replication. In Central European DNA Repair Meeting. 2013.
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Basic information
Original name Exploring synthetic lethal interaction between Checkpoint Kinase 1(CHK1) and DNA replication
Authors SAMADDER, Pounami (356 India, guarantor, belonging to the institution).
Edition Central European DNA Repair Meeting, 2013.
Other information
Original language English
Type of outcome Presentations at conferences
Field of Study 10600 1.6 Biological sciences
Country of publisher Czech Republic
Confidentiality degree is not subject to a state or trade secret
WWW URL
RIV identification code RIV/00216224:14310/13:00076506
Organization unit Faculty of Science
Keywords in English CHK1 DNA repair cancer
Changed by Changed by: Pounami Samadder, Ph.D., učo 404286. Changed: 21/9/2014 10:39.
Abstract
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.
Abstract (in Czech)
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.
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