Chromosome translocations in cancer: computational evidence for the random generation of double-strand breaks

In this article, we show that introns harboring translocation breakpoints in tumors are significantly longer than non-translocated introns of the same genes but are not enriched significantly in sequence elements potentially involved in chromosomal rearrangements. Our findings provide evidence that double-strand breaks, the type of DNA damage that leads to translocations in tumors, are created at random points in the genome, and that sequence elements do not have a widespread role in the localization of these breaks.