Journal
JOURNAL OF MOLECULAR HISTOLOGY
Volume 37, Issue 5-7, Pages 203-218Publisher
SPRINGER
DOI: 10.1007/s10735-006-9043-8
Keywords
DNA repair inhibitors; carcinogenesis; beta-lapachone; DNA repair; NQ01; poly(ADP-ribose) polymerase-1; DNA damage; cancer therapy; cancer prevention
Categories
Funding
- NATIONAL CANCER INSTITUTE [P30CA142543, R01CA102792] Funding Source: NIH RePORTER
- NCI NIH HHS [CA 102792, R01 CA102792, P30 CA142543] Funding Source: Medline
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Defective or abortive repair of DNA lesions has been associated with carcinogenesis. Therefore it is imperative for a cell to accurately repair its DNA after damage if it is to return to a normal cellular phenotype. In certain circumstances, if DNA damage cannot be repaired completely and with high fidelity, it is more advantageous for an organism to have some of its more severely damaged cells die rather than survive as neoplastic transformants. A number of DNA repair inhibitors have the potential to act as anticarcinogenic compounds. These drugs are capable of modulating DNA repair, thus promoting cell death rather than repair of potentially carcinogenic DNA damage mediated by error-prone DNA repair processes. In theory, exposure to a DNA repair inhibitor during, or immediately after, carcinogenic exposure should decrease or prevent tumorigenesis. However, the ability of DNA repair inhibitors to prevent cancer development is difficult to interpret depending upon the system used and the type of genotoxic stress. Inhibitors may act on multiple aspects of DNA repair as well as the cellular signaling pathways activated in response to the initial damage. In this review, we summarize basic DNA repair mechanisms and explore the effects of a number of DNA repair inhibitors that not only potentiate DNA-damaging agents but also decrease carcinogenicity. In particular, we focus on a novel anti-tumor agent, beta-lapachone, and its potential to block transformation by modulating poly(ADP-ribose) polymerase-1.
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