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dc.contributor.authorDura, Polat
dc.contributor.authorBregitha, Caro V V
dc.contributor.authorTe Morsche, Rene H M
dc.contributor.authorRoelofs, Hennie M J
dc.contributor.authorKristinsson, Jon O
dc.contributor.authorWobbes, Theo
dc.contributor.authorWitteman, Ben J M
dc.contributor.authorTan, Adriaan C I T L
dc.contributor.authorDrenth, Joost P H
dc.contributor.authorPeters, Wilbert H M
dc.date.accessioned2013-08-13T13:49:33Z
dc.date.available2013-08-13T13:49:33Z
dc.date.issued2012-06
dc.date.submitted2013-08-13
dc.identifier.citationOncol. Rep. 2012, 27(6):1710-6en_GB
dc.identifier.issn1791-2431
dc.identifier.pmid22447130
dc.identifier.doi10.3892/or.2012.1734
dc.identifier.urihttp://hdl.handle.net/2336/298087
dc.description.abstractEsophageal cancer (EC) has a globally increasing incidence with poor curative treatment options and survival rates. Crucial risk factors are exposure to toxins or carcinogens. Microsomal epoxide hydrolase (mEH) is a biotransformation enzyme essential for the detoxification of xenobiotics. Polymorphisms in exon 3 and exon 4 of the microsomal epoxide hydrolase gene (EPHX1) modify catalytic activity of this enzyme and subsequently may play a role in EC etiology. This case-control study investigated whether these polymorphisms in the EPHX1 gene influence esophageal cancer susceptibility in a Dutch Caucasian population. A case-control study including 349 Caucasian EC patients and 581 Caucasian healthy controls was conducted and the polymorphisms Tyr113His (exon 3) and His139Arg (exon 4) in the EPHX1 gene were determined, using polymerase chain reaction. The distribution of exon 3 and exon 4 genotypes were compared between cases and controls. Analyses included a stratification according to tumor histology; esophageal adenocarcinoma (EAC) or squamous cell carcinoma (ESCC). Furthermore, on the basis of allelic in vitro enzyme activity assays, exon 3 and 4 genotypes were combined and categorized according to their predicted high, medium or low enzyme activity. Homozygosity and heterozygosity for both exon 3 and 4 polymorphisms were correlated with a decreased esophageal squamous cell carcinoma risk. Heterozygosity and homozygosity for both polymorphisms correlated with an increased and a decreased esophageal adenocarcinoma risk, respectively. Predicted intermediate and high activity genotypes were risk and protective factors for esophageal squamous cell carcinoma and esophageal adenocarcinoma, respectively. However, none of these associations were statistically significant. In conclusion, the polymorphisms in exon 3 and exon 4 of the EPHX1 gene do not seem to be modifiers of esophageal squamous cell carcinoma or esophageal adenocarcinoma risk in Dutch Caucasians.
dc.language.isoenen
dc.relation.urlhttp://www.spandidos-publications.com/or/27/6en_GB
dc.relation.urlhttp://dx.doi.org/10.3892/or.2012.1734en_GB
dc.rightsArchived with thanks to Oncology reportsen_GB
dc.subject.meshAdenocarcinomaen_GB
dc.subject.meshAgeden_GB
dc.subject.meshAged, 80 and overen_GB
dc.subject.meshCarcinoma, Squamous Cellen_GB
dc.subject.meshCase-Control Studiesen_GB
dc.subject.meshEpoxide Hydrolasesen_GB
dc.subject.meshEsophageal Neoplasmsen_GB
dc.subject.meshEuropean Continental Ancestry Groupen_GB
dc.subject.meshFemaleen_GB
dc.subject.meshGenetic Predisposition to Diseaseen_GB
dc.subject.meshGenotypeen_GB
dc.subject.meshHeterozygoteen_GB
dc.subject.meshHomozygoteen_GB
dc.subject.meshHumansen_GB
dc.subject.meshMaleen_GB
dc.subject.meshMiddle Ageden_GB
dc.subject.meshNetherlandsen_GB
dc.subject.meshPolymorphism, Single Nucleotideen_GB
dc.subject.meshRisk Factorsen_GB
dc.titleEPHX1 polymorphisms do not modify esophageal carcinoma susceptibility in Dutch Caucasians.en
dc.typeArticleen
dc.contributor.departmentDepartment of Gastroenterology, Radboud University Medical Center, Nijmegen, The Netherlandsen_GB
dc.identifier.journalOncology reportsen_GB
dc.rights.accessOpen Access - Opinn aðganguren
html.description.abstractEsophageal cancer (EC) has a globally increasing incidence with poor curative treatment options and survival rates. Crucial risk factors are exposure to toxins or carcinogens. Microsomal epoxide hydrolase (mEH) is a biotransformation enzyme essential for the detoxification of xenobiotics. Polymorphisms in exon 3 and exon 4 of the microsomal epoxide hydrolase gene (EPHX1) modify catalytic activity of this enzyme and subsequently may play a role in EC etiology. This case-control study investigated whether these polymorphisms in the EPHX1 gene influence esophageal cancer susceptibility in a Dutch Caucasian population. A case-control study including 349 Caucasian EC patients and 581 Caucasian healthy controls was conducted and the polymorphisms Tyr113His (exon 3) and His139Arg (exon 4) in the EPHX1 gene were determined, using polymerase chain reaction. The distribution of exon 3 and exon 4 genotypes were compared between cases and controls. Analyses included a stratification according to tumor histology; esophageal adenocarcinoma (EAC) or squamous cell carcinoma (ESCC). Furthermore, on the basis of allelic in vitro enzyme activity assays, exon 3 and 4 genotypes were combined and categorized according to their predicted high, medium or low enzyme activity. Homozygosity and heterozygosity for both exon 3 and 4 polymorphisms were correlated with a decreased esophageal squamous cell carcinoma risk. Heterozygosity and homozygosity for both polymorphisms correlated with an increased and a decreased esophageal adenocarcinoma risk, respectively. Predicted intermediate and high activity genotypes were risk and protective factors for esophageal squamous cell carcinoma and esophageal adenocarcinoma, respectively. However, none of these associations were statistically significant. In conclusion, the polymorphisms in exon 3 and exon 4 of the EPHX1 gene do not seem to be modifiers of esophageal squamous cell carcinoma or esophageal adenocarcinoma risk in Dutch Caucasians.


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