Morgan W F, Corcoran J, Hartmann A, Kaplan M I, Limoli C L, Ponnaiya B
Departments of Radiation Oncology and Radiology, Box 0750, University of California, San Francisco, CA 94143-0750, USA.
Mutat Res. 1998 Aug 3;404(1-2):125-8. doi: 10.1016/s0027-5107(98)00104-3.
DNA double-strand breaks can lead to chromosomal rearrangements at the first mitosis after exposure to the DNA strand-breaking agent. The evidence suggests a number of different pathways for DNA double-strand break rejoining in mammalian cells, but it is unclear what factors determine the fate of the induced break and whether or not it will lead to chromosomal rearrangement. If a cell does survive and proliferate after DNA cleavage, delayed chromosomal instability can be observed in the clonal descendants of the exposed cell. Most, but not all DNA double-strand breaking agents are effective at inducing this delayed chromosomal instability. In this paper, we review the evidence for the role of the DNA double-strand break in directly induced and delayed chromosomal rearrangements.
