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Mutagenesis Advance Access originally published online on April 4, 2007
Mutagenesis 2007 22(4):247-253; doi:10.1093/mutage/gem009
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© The Author 2007. Published by Oxford University Press. All rights reserved.
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Mutator pathways unleashed by epigenetic silencing in human cancer

Filipe V. Jacinto and Manel Esteller*

Cancer Epigenetics Laboratory, Molecular Pathology Programme, Spanish National Cancer Centre (CNIO), Madrid, Spain

Human cancers exhibit genomic instability and an increased mutation rate due to underlying defects in DNA repair genes. Hypermethylation of CpG islands in gene promoter regions is an important mechanism of gene inactivation in cancer. Many cellular pathways, including DNA repair, are inactivated by this type of epigenetic lesion, resulting in mutator pathways. In this review, we discuss the adverse consequences suffered by a cell when DNA repair genes such as the DNA mismatch repair gene hMLH1, the DNA alkyl-repair gene O6-methylguanine-DNA methyltransferase, the familial breast cancer gene BRCA1 and the Werner syndrome gene WRN become epigenetically silenced in human cancer.

* To whom correspondence should be addressed. Tel: 34 91 2246940; Fax: 34 91 2246923; Email: mesteller{at}cnio.es

Received on January 3, 2007; revised on February 2, 2007; accepted on February 5, 2007.


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