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.
Novo
Francisco J
FJ
Department of Genetics, University of Navarra, 31080, Pamplona, Spain. fnovo@unav.es
Vizmanos
José L
JL
D019457:Chromosome Breakage; D004247:DNA / Q000235:genetics*; D004249:DNA Damage / Q000235:genetics*; D015894:Genome, Human; D006801:Humans; D007438:Introns; D009369:Neoplasms / Q000235:genetics*; D011897:Random Allocation; D014178:Translocation, Genetic
D004247:DNA