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Targeting base excision repair to improve cancer therapies

By Ricky A. Sharma and Grigory L. Dianov

Abstract

This is the authors' final draft of the paper published as Molecular Aspects of Medicine, 2007, 28, pp. 345-374. The final definitive version is available from www.sciencedirect.com, doi:10.1016/j.mam.2007.06.002.Most commonly used cancer therapies, particularly ionizing radiation and certain classes of cytotoxic chemotherapies, cause cell death by damaging DNA. Base excision repair (BER) is the major system responsible for the removal of corrupt DNA bases and repair of DNA single strand breaks generated spontaneously and induced by exogenous DNA damaging factors such as certain cancer therapies. In this review, the physico-chemical properties of the proteins involved in BER are discussed with particular emphasis on molecular mechanisms coordinating repair processes. The aim of this review is to apply extensive knowledge that currently exists regarding the biochemical mechanisms involved in human BER to the molecular biology of current therapies for cancer. It is anticipated that the application of this knowledge will translate into the development of novel effective therapies for improving existing treatments such as radiation therapy and oxaliplatin chemotherapy

Publisher: Elsevier
Year: 2007
DOI identifier: 10.1016/j.mam.2007.06.002
OAI identifier: oai:lra.le.ac.uk:2381/2655

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