Cell cycle checkpoint and DNA damage response defects as anticancer targets: from molecular mechanisms to therapeutic opportunities.

Spoerri, Loredana, Oo, Zay Yar, Larsen, Jill E., Haass, Nikolas K., Gabrielli, Brian and Pavey, Sandra (2015). Cell cycle checkpoint and DNA damage response defects as anticancer targets: from molecular mechanisms to therapeutic opportunities.. In Stress response pathways in cancer: from molecular targets to novel therapeutics (pp. 29-49) Dordrecht: Springer Science+Business Media. doi:10.1007/978-94-017-9421-3_3


Author Spoerri, Loredana
Oo, Zay Yar
Larsen, Jill E.
Haass, Nikolas K.
Gabrielli, Brian
Pavey, Sandra
Title of chapter Cell cycle checkpoint and DNA damage response defects as anticancer targets: from molecular mechanisms to therapeutic opportunities.
Title of book Stress response pathways in cancer: from molecular targets to novel therapeutics
Place of Publication Dordrecht
Publisher Springer Science+Business Media
Publication Year 2015
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1007/978-94-017-9421-3_3
Year available 2015
ISBN 9789401794206
9789401794213
Chapter number 3
Start page 29
End page 49
Total pages 21
Total chapters 18
Collection year 2015
Language eng
Formatted Abstract/Summary
Cells have evolved a DNA damage response (DDR) pathway to monitor the integrity of their genome, which is tightly associated with cell cycle checkpoint controls, arresting cells to allow for DNA repair before continuing through the cell cycle. Defects in the DDR and checkpoint mechanisms frequently occur in human cancers, with failure of the cell to repair the DNA damage leading to genomic instability, increased mutation load, and cellular transformation. The loss of a DNA damage checkpoint in a tumour should make it vulnerable to checkpoint override strategies, providing therapeutic opportunities to inhibit mechanisms that compensate for the defect. Here we review the DDR pathway and cell cycle checkpoint responses to DNA damage, and explain how defects in these mechanisms present a significant opportunity for therapeutic intervention. These defects can be exploited using a synthetic lethal approach to target tumours with these defects and having limited normal tissue toxicity.
Keyword Cell cycle
Mitosis
Checkpoint
Cancer
Chemotherapy
Q-Index Code B1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Book Chapter
Collections: Official 2016 Collection
UQ Diamantina Institute Publications
 
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Created: Fri, 05 Dec 2014, 18:31:46 EST by Nikolas Haass on behalf of UQ Diamantina Institute