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Cancers 2014, 6(3), 1597-1614; doi:10.3390/cancers6031597

DNA Mismatch Repair and Oxidative DNA Damage: Implications for Cancer Biology and Treatment

Centre for Molecular Oncology, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Received: 14 May 2014 / Revised: 2 July 2014 / Accepted: 18 July 2014 / Published: 5 August 2014
(This article belongs to the Special Issue Role of Oxidatively-Induced DNA Damage in Carcinogenesis)
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Many components of the cell, including lipids, proteins and both nuclear and mitochondrial DNA, are vulnerable to deleterious modifications caused by reactive oxygen species. If not repaired, oxidative DNA damage can lead to disease-causing mutations, such as in cancer. Base excision repair and nucleotide excision repair are the two DNA repair pathways believed to orchestrate the removal of oxidative lesions. However, recent findings suggest that the mismatch repair pathway may also be important for the response to oxidative DNA damage. This is particularly relevant in cancer where mismatch repair genes are frequently mutated or epigenetically silenced. In this review we explore how the regulation of oxidative DNA damage by mismatch repair proteins may impact on carcinogenesis. We discuss recent studies that identify potential new treatments for mismatch repair deficient tumours, which exploit this non-canonical role of mismatch repair using synthetic lethal targeting. View Full-Text
Keywords: oxidative DNA damage; mismatch repair; ROS; chemotherapeutics; mitochondria oxidative DNA damage; mismatch repair; ROS; chemotherapeutics; mitochondria

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This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Bridge, G.; Rashid, S.; Martin, S.A. DNA Mismatch Repair and Oxidative DNA Damage: Implications for Cancer Biology and Treatment. Cancers 2014, 6, 1597-1614.

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