Poly(ADP-ribose) polymerase inhibitors as potential chemotherapeutic agents.
PARP [poly(ADP-ribose) polymerase] activity is up-regulated by binding to DNA strand breaks and its association with DNA repair is well documented. Many anticancer therapies work by inducing breaks in DNA, if unrepaired these can lead to cell death. As PARP promotes DNA repair there is a strong rational to suggest that its inhibition may increase the efficiency of certain cytotoxic treatments. This review discusses the advances made in PARP inhibitor design and the mechanism by which they enhance anti-tumour therapies.
Bryant
H E
HE
The Institute for Cancer Studies, University of Sheffield, Medical School, Beech Hill Road, Sheffield S10 2RX, UK.
Helleday
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D000970:Antineoplastic Agents / Q000627:therapeutic use*; D052176:Azulenes; D001569:Benzodiazepines / Q000494:pharmacology; D004261:DNA Replication / Q000187:drug effects; D015195:Drug Design; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D006801:Humans; D000067856:Poly(ADP-ribose) Polymerase Inhibitors
C479234:1-(4-dimethylaminomethylphenyl)-8,9-dihydro-7H-2,7,9a-benzo(cd)azulen-6-one; D000970:Antineoplastic Agents; D052176:Azulenes; D004791:Enzyme Inhibitors; D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D001569:Benzodiazepines