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Int J Mol Sci. 2012;13(9):11974-99. doi: 10.3390/ijms130911974. Epub 2012 Sep 20.

Common fragile sites: genomic hotspots of DNA damage and carcinogenesis.

Author information

  • 1Department of Biochemistry and Molecular Biology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China; E-Mails: nmgdxmark@126.com (K.M.); nangongningchen@163.com (L.Q.); doctorjunzhang@163.com (J.Z.) ; Key Laboratory of Ministry of Education for Breast Cancer Prevention and Treatment, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.

Abstract

Genomic instability, a hallmark of cancer, occurs preferentially at specific genomic regions known as common fragile sites (CFSs). CFSs are evolutionarily conserved and late replicating regions with AT-rich sequences, and CFS instability is correlated with cancer. In the last decade, much progress has been made toward understanding the mechanisms of chromosomal instability at CFSs. However, despite tremendous efforts, identifying a cancer-associated CFS gene (CACG) remains a challenge and little is known about the function of CACGs at most CFS loci. Recent studies of FATS (for Fragile-site Associated Tumor Suppressor), a new CACG at FRA10F, reveal an active role of this CACG in regulating DNA damage checkpoints and suppressing tumorigenesis. The identification of FATS may inspire more discoveries of other uncharacterized CACGs. Further elucidation of the biological functions and clinical significance of CACGs may be exploited for cancer biomarkers and therapeutic benefits.

KEYWORDS:

CFS; FATS; cancer; checkpoint; instability; replication

PMID:
23109895
PMCID:
PMC3472787
DOI:
10.3390/ijms130911974
[PubMed - indexed for MEDLINE]
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