期刊
SEMINARS IN CANCER BIOLOGY
卷 20, 期 5, 页码 353-359出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcancer.2010.10.005
关键词
Lethal mutagenesis; Mutator phenotype; Mutation rate; Cancer genome
类别
资金
- National Cancer Institute [CA102029, CA115802]
- NATIONAL CANCER INSTITUTE [R01CA102029, R01CA115802] Funding Source: NIH RePORTER
The evolution of cancer and RNA viruses share many similarities. Both exploit high levels of genotypic diversity to enable extensive phenotypic plasticity and thereby facilitate rapid adaptation. In order to accumulate large numbers of mutations, we have proposed that cancers express a mutator phenotype. Similar to cancer cells, many viral populations, by replicating their genomes with low fidelity, carry a substantial mutational load. As high levels of mutation are potentially deleterious, the viral mutation frequency is thresholded at a level below which viral populations equilibrate in a traditional mutation-selection balance, and above which the population is no longer viable, i.e., the population undergoes an error catastrophe. Because their mutation frequencies are fine-tuned just below this error threshold, viral populations are susceptible to further increases in mutational load and, recently this phenomenon has been exploited therapeutically by a concept that has been termed lethal mutagenesis. Here we review the application of lethal mutagenesis to the treatment of HIV and discuss how lethal mutagenesis may represent a novel therapeutic approach for the treatment of solid cancers. (C) 2010 Elsevier Ltd. All rights reserved.
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