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• W2047631844 startingPage "5249" @default.
• W2047631844 abstract "In human cells DNA double strand breaks (DSBs) can be repaired by the non-homologous end-joining (NHEJ) pathway. In a background of NHEJ deficiency, DSBs with mismatched ends can be joined by an error-prone mechanism involving joining between regions of nucleotide microhomology. The majority of joins formed from a DSB with partially incompatible 3′ overhangs by cell-free extracts from human glioblastoma (MO59K) and urothelial (NHU) cell lines were accurate and produced by the overlap/fill-in of mismatched termini by NHEJ. However, repair of DSBs by extracts using tissue from four high-grade bladder carcinomas resulted in no accurate join formation. Junctions were formed by the non-random deletion of terminal nucleotides and showed a preference for annealing at a microhomology of 8 nt buried within the DNA substrate; this process was not dependent on functional Ku70, DNA-PK or XRCC4. Junctions were repaired in the same manner in MO59K extracts in which accurate NHEJ was inactivated by inhibition of Ku70 or DNA-PKcs. These data indicate that bladder tumour extracts are unable to perform accurate NHEJ such that error-prone joining predominates. Therefore, in high-grade tumours mismatched DSBs are repaired by a highly mutagenic, microhomology-mediated, alternative end-joining pathway, a process that may contribute to genomic instability observed in bladder cancer." @default.
• W2047631844 created "2016-06-24" @default.
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• W2047631844 date "2004-09-23" @default.
• W2047631844 modified "2023-09-26" @default.
• W2047631844 title "DNA double strand break repair in human bladder cancer is error prone and involves microhomology-associated end-joining" @default.
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• W2047631844 doi "https://doi.org/10.1093/nar/gkh842" @default.
• W2047631844 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/521655" @default.
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