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Nucleic Acids Research 2006 34(3):840-852; doi:10.1093/nar/gkj489
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Published online 6 February 2006

© The Author 2006. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions{at}oxfordjournals.org

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Molecular models for the tissue specificity of DNA mismatch repair-deficient carcinogenesis

Elizabeth C. Chao1,2,* and Steven M. Lipkin1,2

1Department of Medicine, Divisions of Hematology-Oncology and Epidemiology, University of California Irvine, CA 92697-4038, USA 2Department of Biological Chemistry, Divisions of Hematology-Oncology and Epidemiology, University of California Irvine, CA 92697-4038, USA

*To whom correspondence should be addressed. Tel: +1 949 824 9221; Fax: +1 949 824 9224; Email: ecchao{at}uci.edu

Received August 23, 2005. Revised November 17, 2005. Accepted January 18, 2006.

A common feature of all the known cancer genetic syndromes is that they predispose only to selective types of malignancy. However, many of the genes mutated in these syndromes are ubiquitously expressed, and influence seemingly universal processes such as DNA repair or cell cycle control. The tissue specificity of cancers that arise from malfunction of these apparently universal traits remains a key puzzle in cancer genetics. Mutations in DNA mismatch repair (MMR) genes cause the most common known cancer genetic syndrome, hereditary non-polyposis colorectal cancer, and the fundamental biology of MMR is one of the most intensively studied processes in laboratories all around the world. This review uses MMR as a model system to understand mechanisms that may explain the selective development of tumors in particular cell types despite the universal nature of this process. We evaluate recent data giving insights into the specific tumor types that are attributable to defective MMR in humans and mice under different modes of inheritance, and propose models that may explain the spectrum of cancer types observed.

Correspondence may also be addressed to Steven M. Lipkin. Email: slipkin{at}uci.edu


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