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Journal of Biomedicine and Biotechnology
Volume 2011 (2011), Article ID 984505, 10 pages
Review Article

Common Fragile Site Tumor Suppressor Genes and Corresponding Mouse Models of Cancer

1Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, OH 43210 , USA
2Clinical Pathology, Regina Elena Institute, IFO, 00144 Rome, Italy
3 Department of Immunology and Cancer Research-IMRIC, The Lautenberg Center for General and Tumor Immunology, Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel

Received 14 September 2010; Accepted 23 November 2010

Academic Editor: Monica Fedele

Copyright © 2011 Alessandra Drusco et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Chromosomal common fragile sites (CFSs) are specific mammalian genomic regions that show an increased frequency of gaps and breaks when cells are exposed to replication stress in vitro. CFSs are also consistently involved in chromosomal abnormalities in vivo related to cancer. Interestingly, several CFSs contain one or more tumor suppressor genes whose structure and function are often affected by chromosomal fragility. The two most active fragile sites in the human genome are FRA3B and FRA16D where the tumor suppressor genes FHIT and WWOX are located, respectively. The best approach to study tumorigenic effects of altered tumor suppressors located at CFSs in vivo is to generate mouse models in which these genes are inactivated. This paper summarizes our present knowledge on mouse models of cancer generated by knocking out tumor suppressors of CFS.