Linked Life Data

15598760

Source:http://linkedlifedata.com/resource/pubmed/id/15598760

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2004-12-15
pubmed:abstractText
DNA repair is essential to an individual's ability to respond to damage caused by environmental carcinogens. Alterations in DNA repair genes may affect cancer risk by influencing individual susceptibility to environmental exposures. XPD, a gene involved in nucleotide excision repair, may influence individual DNA repair capacity particularly of bulky adducts. Using a population-based breast cancer case-control study that was specifically conducted to examine markers of environmental exposures, such as polycyclic aromatic hydrocarbons (PAH), on Long Island, NY, we examined whether XPD genotype modified the associations among PAH-DNA adducts, cigarette smoking, and breast cancer risk. Specifically, we examined the XPD polymorphism at exon 23, position 751 in 1,053 breast cancer cases and 1,102 population-based controls. The presence of at least one variant allele (Lys/Gln or Gln/Gln) was associated with a 20% increase in risk of breast cancer [odds ratio (OR), 1.21; 95% confidence interval (95% CI), 1.01-1.44]. The increase in risk for homozygosity of the variant allele (Gln/Gln) seemed limited to those with PAH-DNA adduct levels above the median(OR, 1.61; 95% CI, 0.99-2.63 for adducts above the median versus OR, 1.05; 95% CI, 0.64-1.74 for adductsbelow the median), although the multiplicative interaction was not statistically significant. The increasein risk for homozygosity of the variant allele (Gln/Gln) was only seen among current smokers (OR, 1.97; 95% CI, 1.02-3.81 for current smokers versus OR, 0.87; 95% CI, 0.57-1.32 for never smokers); the multiplicative interaction was statistically significant. Overall, this study suggests that those individuals with this polymorphism in the XPD gene may face an increased risk of breast cancer from PAH-DNA adducts and cigarette smoking.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1055-9965
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2053-8
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:15598760-Adult, pubmed-meshheading:15598760-Aged, pubmed-meshheading:15598760-Breast Neoplasms, pubmed-meshheading:15598760-Case-Control Studies, pubmed-meshheading:15598760-DNA Adducts, pubmed-meshheading:15598760-DNA Helicases, pubmed-meshheading:15598760-DNA Repair, pubmed-meshheading:15598760-DNA-Binding Proteins, pubmed-meshheading:15598760-Environmental Exposure, pubmed-meshheading:15598760-Female, pubmed-meshheading:15598760-Genetic Predisposition to Disease, pubmed-meshheading:15598760-Genotype, pubmed-meshheading:15598760-Humans, pubmed-meshheading:15598760-Middle Aged, pubmed-meshheading:15598760-New York, pubmed-meshheading:15598760-Odds Ratio, pubmed-meshheading:15598760-Polycyclic Hydrocarbons, Aromatic, pubmed-meshheading:15598760-Polymorphism, Genetic, pubmed-meshheading:15598760-Smoking, pubmed-meshheading:15598760-Transcription Factors, pubmed-meshheading:15598760-Xeroderma Pigmentosum Group D Protein
pubmed:year
2004
pubmed:articleTitle
Polymorphism in the DNA repair gene XPD, polycyclic aromatic hydrocarbon-DNA adducts, cigarette smoking, and breast cancer risk.
pubmed:affiliation
Department of Epidemiology, Mailman School of Public Health, Columbia University, PH 18-102, 600 West 168th Street, New York, NY 10032, USA. mt146@columbia.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't