Telomere dysfunction provokes regional amplification and deletion in cancer genomes

摘要: Telomere dysfunction and associated fusion-breakage in the mouse encourages epithelial carcinogenesis a more humanized genomic profile that includes nonreciprocal translocations (NRTs). Here, array comparative hybridization was used to determine pathogenic significance of NRTs whether telomere also drives amplifications deletions cancer-relevant loci. Compared tumors arising mice with intact telomeres, possessed higher levels instability showed numerous regions syntenic human cancer hotspots. These observations suggest telomere-based crisis provides mechanism chromosomal instability, including regional deletions, carcinogenesis. This model platform for discovery genes responsible major cancers affecting aged humans.