DNA double-strand break repair pathways, chromosomal rearrangements and cancer.
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 replicatio...
| Main Authors: | , |
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| Format: | Journal article |
| Language: | English |
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2011
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| _version_ | 1797076197838946304 |
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| author | Kasparek, T Humphrey, T |
| author_facet | Kasparek, T Humphrey, T |
| author_sort | Kasparek, T |
| collection | OXFORD |
| description | 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. |
| first_indexed | 2024-03-07T00:00:43Z |
| format | Journal article |
| id | oxford-uuid:75d7d973-2e8d-4967-846e-12fd30a09e98 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T00:00:43Z |
| publishDate | 2011 |
| record_format | dspace |
| spelling | oxford-uuid:75d7d973-2e8d-4967-846e-12fd30a09e982022-03-26T20:11:55ZDNA double-strand break repair pathways, chromosomal rearrangements and cancer.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:75d7d973-2e8d-4967-846e-12fd30a09e98EnglishSymplectic Elements at Oxford2011Kasparek, THumphrey, TChromosomal 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. |
| spellingShingle | Kasparek, T Humphrey, T DNA double-strand break repair pathways, chromosomal rearrangements and cancer. |
| title | DNA double-strand break repair pathways, chromosomal rearrangements and cancer. |
| title_full | DNA double-strand break repair pathways, chromosomal rearrangements and cancer. |
| title_fullStr | DNA double-strand break repair pathways, chromosomal rearrangements and cancer. |
| title_full_unstemmed | DNA double-strand break repair pathways, chromosomal rearrangements and cancer. |
| title_short | DNA double-strand break repair pathways, chromosomal rearrangements and cancer. |
| title_sort | dna double strand break repair pathways chromosomal rearrangements and cancer |
| work_keys_str_mv | AT kasparekt dnadoublestrandbreakrepairpathwayschromosomalrearrangementsandcancer AT humphreyt dnadoublestrandbreakrepairpathwayschromosomalrearrangementsandcancer |