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pubmed-article:7692269pubmed:abstractTextDefects in loci on chromosome 11 have been associated with tumourigenicity, anchorage-independent growth, metastasis and radiosensitive DNA repair in tumour cells. The introduction of normal chromosome 11 into these cells suppresses these responses. In the present study we tested two hypotheses: (1) that microcell fusion of normal chromosome 11 into bladder-carcinoma cells (A1698) can protect the cells against chromosomal damage by oxidative stress; and (2) that insertion of normal chromosome 11 corrects a single-strand (SS) DNA-repair defect. Cultures of A1698 (termed parent) and its microcell-mediated hybrid (termed hybrid) were exposed for 1 h to xanthine/xanthine oxidase (X/XO) or co-incubated with human neutrophils activated with 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Micronucleus frequencies (an indication of chromosomal damage) were significantly higher in parent cultures after treatment than in hybrid (P < 0.0001). The level of single-strand DNA breakage and its repair was assayed in X/XO-treated cultures with the alkaline comet assay. There was no significant difference between parent and hybrid in the amount of SS DNA breakage at treatment (P > 0.1) or after 20 min of repair (P > 0.1). The data support the involvement of a defect in chromosome 11 leading to sensitivity to oxidative stress and suggest this defect is not in the initial amount or rate of rejoining of SS DNA breakage.lld:pubmed
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pubmed-article:7692269pubmed:pagination299-308lld:pubmed
pubmed-article:7692269pubmed:dateRevised2007-11-15lld:pubmed
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pubmed-article:7692269pubmed:articleTitleA sensitivity to oxidative stress is linked to chromosome 11 but is not due to a difference in single strand DNA breakage or repair.lld:pubmed
pubmed-article:7692269pubmed:affiliationBritish Columbia Cancer Research Centre, Vancouver, Canada.lld:pubmed
pubmed-article:7692269pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:7692269pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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