Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2008-1-29
pubmed:abstractText
The consumption of alcohol, tobacco and betel quid has been found to be an important contributor to esophageal squamous cell carcinoma (ESCC) in Taiwan. The genotoxic effect of the ADH1B and ALDH2 genes modulating an individual's alcohol-metabolizing capacity on ESCC may be linked to drinking behavior, intake pattern and other exogenous factors. To investigate the interplay of these genetic and environmental factors in determining the risk of ESCC, a multicenter case-control study was conducted. Here, 406 patients with pathology-proven ESCC, as well as 656 gender, age and study hospital matched controls were recruited. Genetic polymorphisms of ADH1B and ALDH2 appeared to correlate with the abstinence of alcohol, though not with tobacco and betel quid. Within the same levels of alcohol consumption, carcinoma risks increased along with an increase in the numbers of ADH1B*1 and ALDH2*2 alleles. The inactive ALDH2*1/*2 genotype was found to multiplicatively interact with a low-to-moderate (0.1-30 g/day) and a heavy (>30 g/day) ethanol intake to increase the ESCC risk (the joint aOR = 14.5 and 102.6, respectively). Among low-to-moderate drinkers, a smoking-dependent carcinogenetic effect for the ADH1B*1/*1 and ALDH2*1/*2+*2/*2 genotypes was recognized, with significant risks found in smokers, but not in nonsmokers. Further, a supra-multiplicative combined risk of ESCC for alcohol and tobacco use was identified among carriers of the ADH1B*1/*1 genotype (p for interaction = 0.042). In conclusion, the interplay of the ADH1B and ALDH2 genotypes, in conjunction with a behaved drinking habit and a practiced drinking pattern, along with continued tobacco consumption, plays an important pathogenic role in modulating ESCC risk.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1097-0215
pubmed:author
pubmed:copyrightInfo
(c) 2007 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
122
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1347-56
pubmed:meshHeading
pubmed-meshheading:18033686-Adult, pubmed-meshheading:18033686-Aged, pubmed-meshheading:18033686-Alcohol Dehydrogenase, pubmed-meshheading:18033686-Alcohol Drinking, pubmed-meshheading:18033686-Aldehyde Dehydrogenase, pubmed-meshheading:18033686-Alleles, pubmed-meshheading:18033686-Areca, pubmed-meshheading:18033686-Base Sequence, pubmed-meshheading:18033686-Carcinogens, pubmed-meshheading:18033686-Carcinoma, Squamous Cell, pubmed-meshheading:18033686-Case-Control Studies, pubmed-meshheading:18033686-DNA Primers, pubmed-meshheading:18033686-Esophageal Neoplasms, pubmed-meshheading:18033686-Ethnic Groups, pubmed-meshheading:18033686-Female, pubmed-meshheading:18033686-Genotype, pubmed-meshheading:18033686-Humans, pubmed-meshheading:18033686-Male, pubmed-meshheading:18033686-Middle Aged, pubmed-meshheading:18033686-Risk Factors, pubmed-meshheading:18033686-Smoking
pubmed:year
2008
pubmed:articleTitle
Carcinogenetic impact of ADH1B and ALDH2 genes on squamous cell carcinoma risk of the esophagus with regard to the consumption of alcohol, tobacco and betel quid.
pubmed:affiliation
Faculty of Public Health, Kaohsiung Medical University, Kaohsiung, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Multicenter Study