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- W47328400 endingPage "53" @default.
- W47328400 startingPage "29" @default.
- W47328400 abstract "This chapter focuses on the base excision repair (BER) pathway which is responsible for the repair of single-base lesions and can be reconstituted in vitro with a glycosylase, AP endonuclease, polymerase β, and a ligase. BER is the predominant pathway for the repair of oxidative and alkylation DNA damage as well as a basic or baseless sites. Without this balance of enzymatic activities, incomplete processing of the damage occurs, repair intermediates accumulate, and eventually cells will die. Inhibition of proliferation and cell death are desirable in tumor cell populations, therefore inhibitors of BER proteins are under development and currently being evaluated in the clinic. Several of these agents are being evaluated in combination with numerous existing chemotherapeutic agents and radiation therapy. Combination therapy with agents that generate DNA damage that is repaired by BER is reasonable and demonstrating efficacy both preclinically and in early clinical trials." @default.
- W47328400 created "2016-06-24" @default.
- W47328400 creator A5029443104 @default.
- W47328400 creator A5055500811 @default.
- W47328400 date "2012-01-01" @default.
- W47328400 modified "2023-09-26" @default.
- W47328400 title "Blockade of Base Excision Repair" @default.
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