Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2005-6-23
pubmed:abstractText
Lack of functional telomeres can cause chromosomal aberrations. This type of genetic instability may promote tumorigenesis. We have investigated the association between mean telomere length in buccal cells (assessed with quantitative real-time PCR) and bladder cancer risk in a case-control study. Patients with bladder cancer displayed significantly shorter telomeres than control subjects (P = 0.001). Median telomere length ratio was 0.95 (range 0.53-3.2) for cases and 1.1 (0.51-2.4) for controls. Moreover, the adjusted odds ratio (OR) for bladder cancer was significantly increased in the quartile with the shortest telomere length OR = 4.5 [95% confidence interval (CI) 1.7-12]. It is known that oxidative stress, alkylation or UV radiation increases shortening of telomeres. Therefore, we also analyzed whether environmental and genetic factors associated with DNA damage, i.e. smoking and polymorphisms in the genes involved in the metabolism of genotoxic carcinogens (EPHX1, GSTA1, GSTM1, GSTP1, GSTT1, NAT1, NAT2 and NQO1) or DNA repair (APE1, NBS1, XPC, XPD, XRCC1, XRCC3 and XRCC4), could modify the association between telomere length and cancer risk. A clear effect of smoking and telomere length could be observed. Current smokers with short telomeres had more than six times as higher risk as non-smokers/former smokers with long telomeres (OR = 6.3, 95% CI 1.7-23). Lack of the biotransformation gene GSTM1 and short telomeres were associated with OR = 6.5 (95% CI 2.4-18), whereas homozygous carriers of 312Asn in the DNA repair gene XPD, with short telomeres, displayed an OR of 17 (95% CI 1.9-150). However, no significant interaction for cancer risk could be proven for telomere length, smoking and susceptibility genotypes of metabolizing and DNA-repairing genes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0143-3334
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1263-71
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15746160-Adult, pubmed-meshheading:15746160-Aged, pubmed-meshheading:15746160-Aged, 80 and over, pubmed-meshheading:15746160-Carcinogens, pubmed-meshheading:15746160-Case-Control Studies, pubmed-meshheading:15746160-DNA Damage, pubmed-meshheading:15746160-DNA Repair, pubmed-meshheading:15746160-Female, pubmed-meshheading:15746160-Genetic Markers, pubmed-meshheading:15746160-Genetic Predisposition to Disease, pubmed-meshheading:15746160-Genotype, pubmed-meshheading:15746160-Glutathione Transferase, pubmed-meshheading:15746160-Humans, pubmed-meshheading:15746160-Male, pubmed-meshheading:15746160-Middle Aged, pubmed-meshheading:15746160-Odds Ratio, pubmed-meshheading:15746160-Polymerase Chain Reaction, pubmed-meshheading:15746160-Risk Factors, pubmed-meshheading:15746160-Smoking, pubmed-meshheading:15746160-Telomere, pubmed-meshheading:15746160-Urinary Bladder Neoplasms
pubmed:year
2005
pubmed:articleTitle
Constitutional short telomeres are strong genetic susceptibility markers for bladder cancer.
pubmed:affiliation
Department of Occupational and Environmental Medicine, Lund University, Sweden. karin.broberg@ymed.lu.se
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't