Linked Life Data

14612556

Source:http://linkedlifedata.com/resource/pubmed/id/14612556

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
21
pubmed:dateCreated
2003-11-12
pubmed:abstractText
Bladder cancer is associated with smoking, occupational exposures, and glutathione S-transferase (GST) M1 and N-acetyltransferase (NAT) 2 polymorphisms that may influence carcinogen metabolism, but somatic p53mutations are often CpG dinucleotide G:C-A:T transitions that can occur spontaneously. We conducted a case-control study to determine whether p53mutation characteristics might distinguish cases with environmental versus endogenous causes. p53exons 4-9 were amplified from 146 bladder tumors by PCR, screened by single-strand conformational polymorphism analysis, and sequenced. Thirty-one cases were p53-positive, and 112 were p53-negative (germ line or silent). G:C-A:T transitions were also subclassified as CpG or non-CpG. Cases and 215 clinic controls were interviewed. GSTM1, NAT1, and NAT2 polymorphisms were assayed from peripheral blood. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using logistic and polytomous regression. Case-control ORs for smoking, occupations, and NAT1*10genotype were similar for p53-positive and p53-negative cases. Associations with GSTM1-null and NAT2-slow genotypes were somewhat stronger for p53-positive [OR, 3.3; CI, 1.4-7.8 (GSTM1 null); OR, 1.8; CI, 0.8-4.0 (NAT2 slow)] than p53-negative cases [OR, 1.5; CI:0.9-2.3 (GSTM1 null); OR, 0.9; CI, 0.6-1.4 (NAT2 slow)]. Smoking was strongly associated with CpG G:C-A:T (OR, 15.3; CI:3.6-65) versus other G:C-A:T (OR, 1.8; CI, 0.3-9.8). NAT2 slow genotypes were also associated with CpG G:C-A:T (OR, 6.2; CI:0.7-52), whereas GSTM1 null was associated with non-CpG G:C-A:T (OR, 7.8; CI, 0.9-65). Associations were not substantially different for case subtypes defined by p53mutation status alone. Estimates for p53 subtypes were imprecise but support in vitro evidence that some CpG G:C-A:T transitions may be caused by smoking and other environmental mutagens.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7530-8
pubmed:dateRevised
2010-9-8
pubmed:meshHeading
pubmed-meshheading:14612556-Acetyltransferases, pubmed-meshheading:14612556-Aged, pubmed-meshheading:14612556-Arylamine N-Acetyltransferase, pubmed-meshheading:14612556-Carcinoma, Transitional Cell, pubmed-meshheading:14612556-Case-Control Studies, pubmed-meshheading:14612556-Female, pubmed-meshheading:14612556-Genes, p53, pubmed-meshheading:14612556-Genetic Predisposition to Disease, pubmed-meshheading:14612556-Glutathione Transferase, pubmed-meshheading:14612556-Humans, pubmed-meshheading:14612556-Isoenzymes, pubmed-meshheading:14612556-Male, pubmed-meshheading:14612556-Middle Aged, pubmed-meshheading:14612556-Mutation, pubmed-meshheading:14612556-Occupational Exposure, pubmed-meshheading:14612556-Polymorphism, Genetic, pubmed-meshheading:14612556-Risk Factors, pubmed-meshheading:14612556-Sex Factors, pubmed-meshheading:14612556-Smoking, pubmed-meshheading:14612556-Urinary Bladder Neoplasms
pubmed:year
2003
pubmed:articleTitle
p53 mutations in bladder cancer: evidence for exogenous versus endogenous risk factors.
pubmed:affiliation
Epidemiology Branch, National Institute of Environmental Health Sciences/NIH, 111 Alexander Drive, Research Triangle Park, North Carolina 27709, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.