Linked Life Data

7692269

Source:http://linkedlifedata.com/resource/pubmed/id/7692269

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-11-5
pubmed:abstractText
Defects 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0027-5107
pubmed:author
pubmed:issnType
Print
pubmed:volume
294
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
299-308
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
A sensitivity to oxidative stress is linked to chromosome 11 but is not due to a difference in single strand DNA breakage or repair.
pubmed:affiliation
British Columbia Cancer Research Centre, Vancouver, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't