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Enhancement of Chemotherapeutic Efficacy by Small Molecule Inhibition of NF-κ B and Checkpoint Kinases

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Apoptosis or programmed cell death is a cellular mechanism used to regulate cell number and eliminate damaged or mutated cells. Many chemotherapeutic agents and ionizing radiation induce not only apoptotic signaling pathways, but also survival responses such as DNA damage responses and cell cycle arrest, which allow for DNA repair. These survival responses determine the toxicity as well as the efficacy of the cancer treatment. Two main DNA damage responses include the activation of the anti-apoptotic transcription factor NF-κB and the activation of cell cycle checkpoint kinases. Strategies of combining chemotherapeutics with (a) inhibitors of NF-κB or (b) inhibitors of checkpoint kinases, may therefore enhance the efficacy of current cancer therapies. This review will be focused on recent progress made in combining traditional chemotherapeutic drugs with small molecule inhibitors of NF-κB and the checkpoint kinases, Chk1 and Chk2.

Keywords: Chemotherapy; IκB; NF-κB; cancer; checkpoint kinase I (Chk1); checkpoint kinases; inhibition; potentiation; proteasome; sensitization

Document Type: Research Article


Affiliations: Department of Chemistry, Michigan State University, East Lansing, MI, USA.

Publication date: 2007-04-01

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  • Current Medicinal Chemistry covers all the latest and outstanding developments in medicinal chemistry and rational drug design. Each issue contains a series of timely in-depth reviews written by leaders in the field covering a range of the current topics in medicinal chemistry. Current Medicinal Chemistry is an essential journal for every medicinal chemist who wishes to be kept informed and up-to-date with the latest and most important developments.
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