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- W2076945188 endingPage "897" @default.
- W2076945188 startingPage "886" @default.
- W2076945188 abstract "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." @default.
- W2076945188 created "2016-06-24" @default.
- W2076945188 creator A5081023176 @default.
- W2076945188 creator A5084880539 @default.
- W2076945188 date "2011-10-01" @default.
- W2076945188 modified "2023-10-09" @default.
- W2076945188 title "DNA double-strand break repair pathways, chromosomal rearrangements and cancer" @default.
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