The complex basis underlying common fragile site instability in cancer

Efrat Ozeri-Galai, Assaf C. Bester, Batsheva Kerem*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

68 Scopus citations


Common fragile sites (CFSs) were characterized almost 30 years ago as sites undergoing genomic instability in cancer. Recently, . in vitro studies have found that oncogene-induced replication stress leads to CFS instability. . In vivo, CFSs were found to be preferentially unstable during early stages of cancer development and to leave a unique signature of instability. It is now increasingly clear that, along the spectrum of replication features characterizing CFSs, failure of origin activation is a common feature. This and other features of CFSs, together with the replication stress characterizing early stages of cancer development, lead to incomplete replication that results in genomic instability preferentially at CFSs. Here, we review the shared and unique characteristics of CFSs, their underlying causes and their implications, particularly with respect to the development of cancer.

Original languageAmerican English
Pages (from-to)295-302
Number of pages8
JournalTrends in Genetics
Issue number6
StatePublished - Jun 2012


  • Cancer
  • DNA damage
  • Dormant origins
  • Fragile sites
  • Genomic instability
  • Replication


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