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Chromosomal rearrangements, which can lead to oncogene activation and tumour suppressor loss, are a hallmark of cancer cells. Such outcomes can result from both the repair and misrepair of DNA ends, which arise from a variety of lesions including DNA double strand breaks (DSBs), collapsed replication forks and dysfunctional telomeres. Here we review the mechanisms by which non-homologous end joining (NHEJ) and homologous recombination (HR) repair pathways can both promote chromosomal rearrangements and also suppress them in response to such lesions, in accordance with their increasingly recognised tumour suppressor function. Further, we consider how chromosomal rearrangements, together with a modular approach towards understanding their etiology, may be exploited for cancer therapy.

Original publication

DOI

10.1016/j.semcdb.2011.10.007

Type

Journal article

Journal

Semin Cell Dev Biol

Publication Date

10/2011

Volume

22

Pages

886 - 897

Keywords

Chromosome Aberrations, DNA Breaks, Double-Stranded, DNA Repair, Humans, Neoplasms