Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-4-5
pubmed:abstractText
NAT2 (arylamine N-acetyltransferase 2) polymorphism, being a key determinant of individual variations in acetylation capacity, is suspected to modify the risk of carcinogen-related malignancies. As tobacco smoke and other inhaled hazards contain a variety of NAT2 substrates, the relationship between NAT2 phenotype and lung cancer (LC) risk has been a subject of intensive research, however different case-control studies produced controversial data. In the present report, we employed a novel 'comparison of extremes' approach, i.e. we compared the distribution of NAT2 genotypes in lung cancer patients (LC, n=178) not only to the population controls (healthy donors (HD), n=364), but also to the subjects with a putative cancer-resistant constitution (elderly tumor-free smokers and non-smokers (ED), n=351). Frequencies of homozygous rapid, heterozygous rapid and slow acetylators were 6, 39 and 56% in LC, 8, 32 and 60% in HD, and 6, 35 and 59% in ED, respectively. Comparison of the NAT2 genotype frequencies between affected and non-affected individuals did not reveal any statistical deviations, irrespectively of smoking history, gender, age, or histological type of LC. Adjusted odds ratio for rapid vs. slow acetylators was 1.12 (95% confidence intervals (CI): 0.73-1.74) comparing LC vs. HD, and 1.10 (95% CI: 0.74-1.62) comparing LC vs. ED. Similar distribution of NAT2 acetylator genotypes both in tumor-prone and in tumor-resistant groups suggests that, despite the presence of NAT2 carcinogenic substrates in tobacco smoke, NAT2 polymorphism does not play a noticeable role in lung cancer susceptibility.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0304-3835
pubmed:author
pubmed:issnType
Print
pubmed:day
28
pubmed:volume
221
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
177-83
pubmed:dateRevised
2010-9-8
pubmed:meshHeading
pubmed-meshheading:15808403-Acetylation, pubmed-meshheading:15808403-Adolescent, pubmed-meshheading:15808403-Adult, pubmed-meshheading:15808403-Aged, pubmed-meshheading:15808403-Aged, 80 and over, pubmed-meshheading:15808403-Arylamine N-Acetyltransferase, pubmed-meshheading:15808403-Carcinoma, Non-Small-Cell Lung, pubmed-meshheading:15808403-Carcinoma, Small Cell, pubmed-meshheading:15808403-Carcinoma, Squamous Cell, pubmed-meshheading:15808403-Female, pubmed-meshheading:15808403-Gene Frequency, pubmed-meshheading:15808403-Genetic Predisposition to Disease, pubmed-meshheading:15808403-Genotype, pubmed-meshheading:15808403-Heterozygote, pubmed-meshheading:15808403-Homozygote, pubmed-meshheading:15808403-Humans, pubmed-meshheading:15808403-Lung Neoplasms, pubmed-meshheading:15808403-Male, pubmed-meshheading:15808403-Middle Aged, pubmed-meshheading:15808403-Odds Ratio, pubmed-meshheading:15808403-Polymorphism, Genetic, pubmed-meshheading:15808403-Risk Factors, pubmed-meshheading:15808403-Smoking, pubmed-meshheading:15808403-Tumor Markers, Biological
pubmed:year
2005
pubmed:articleTitle
'Comparison of extremes' approach provides evidence against the modifying role of NAT2 polymorphism in lung cancer susceptibility.
pubmed:affiliation
Group of Molecular Diagnostics, N.N. Petrov Institute of Oncology, Pesochny-2, St-Petersburg 197758, Russian Federation.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't