Published online February 18, 2008
doi:10.1083/jcb.200801030
The Journal of Cell Biology, Vol. 180, No. 4, 661-663
The Rockefeller University Press, 0021-9525 $30.00
© 2008 Yuen et al.
The wages of CIN
Karen W. Yuen1,2 and
Arshad Desai1,2
1 Ludwig Institute for Cancer Research and 2 Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093
Correspondence to Karen W. Yuen: kayuen{at}ucsd.edu; or Arshad Desai: abdesai{at}ucsd.edu
Aneuploidy and chromosome instability (CIN) are hallmarks of the majority of solid tumors, but the relationship between them is not well understood. In this issue, Thompson and Compton (Thompson, S.L., and D.A. Compton. 2008. Examining the link between chromosomal instability and aneuploidy in human cells. J. Cell. Biol. 180:665–672) investigate the mechanism of CIN in cancer cells and find that CIN arises primarily from defective kinetochore–spindle attachments that evade detection by the spindle checkpoint and persist into anaphase. They also explore the consequences of artificially elevating chromosome missegregation in otherwise karyotypically normal cells. Their finding that induced aneuploidy is rapidly selected against suggests that the persistence of aneuploid cells in tumors requires not only chromosome missegregation but also additional, as yet poorly defined events.

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Examining the link between chromosomal instability and aneuploidy in human cells
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J. Cell Biol. 2008 180: 665-672.
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