Polymorphisms in DNA repair genes in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma
To test the hypothesis that aberrations of DNA repair contribute to susceptibility for the progression of gastroesophageal reflux disease (GERD) into Barrett esophagus (BE) and esophageal adenocarcinoma (EADC), we studied the frequency of polymorphisms of selected DNA repair genes in patients with G...
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| Veröffentlicht in: | Carcinogenesis (New York) 2005-09, Vol.26 (9), p.1536-1541 |
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| creator | Casson, Alan G. Zheng, Zuoyu Evans, Susan C. Veugelers, Paul J. Porter, Geoffrey A. Guernsey, Duane L. |
| description | To test the hypothesis that aberrations of DNA repair contribute to susceptibility for the progression of gastroesophageal reflux disease (GERD) into Barrett esophagus (BE) and esophageal adenocarcinoma (EADC), we studied the frequency of polymorphisms of selected DNA repair genes in patients with GERD (n = 126), BE (n = 125) and EADC (n = 56) enrolled in a 2-year prospective case–control study. Controls comprised 95 strictly asymptomatic healthy individuals. Using genomic DNA extracted from blood samples, we identified wild-type and polymorphic variants of XPD (Arg156Arg and Lys751Gln), XRCC1 (Arg194Trp and Arg399Gln) and XRCC3 (Thr241Met), and the poly (AT) insertion/deletion of XPC (PAT). Allelic frequencies were compared between cases and controls using logistic regression to calculate age, gender, smoking and alcohol-adjusted odds ratios (OR) and 95% confidence intervals (CI). Patients with EADC demonstrated a significantly higher frequency of the XPC PAT homozygous variant genotype compared with asymptomatic controls (OR = 3.82; 95% CI = 1.05–13.93). Significantly reduced frequencies were seen for the XPD Lys751Gln homozygous variant genotype in patients with EADC (OR = 0.24; 95% CI = 0.07–0.88), and for the XRCC1 Arg399Gln homozygous variant genotype in patients with BE (OR = 0.38; 95% CI = 0.12–0.64) and GERD (OR = 0.29; 95% CI = 0.12–0.66). We conclude that the malignant phenotype probably results from a summation of polymorphic nucleotide excision repair genes showing opposing effects (an increased risk of XPC versus a protective effect of XPD). The protective effect of the homozygous variant of XRCC1 Arg399Gln for GERD and BE suggests that base excision repair alterations may occur early in progression to EADC, likely in response to GERD-induced endogenous oxidative or inflammatory DNA damage. As GERD and BE are highly prevalent in the general population, this protective effect may well explain why only a fraction of individuals with GERD and BE progress into invasive EADC. |
| doi_str_mv | 10.1093/carcin/bgi115 |
| format | Article |
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Controls comprised 95 strictly asymptomatic healthy individuals. Using genomic DNA extracted from blood samples, we identified wild-type and polymorphic variants of XPD (Arg156Arg and Lys751Gln), XRCC1 (Arg194Trp and Arg399Gln) and XRCC3 (Thr241Met), and the poly (AT) insertion/deletion of XPC (PAT). Allelic frequencies were compared between cases and controls using logistic regression to calculate age, gender, smoking and alcohol-adjusted odds ratios (OR) and 95% confidence intervals (CI). Patients with EADC demonstrated a significantly higher frequency of the XPC PAT homozygous variant genotype compared with asymptomatic controls (OR = 3.82; 95% CI = 1.05–13.93). Significantly reduced frequencies were seen for the XPD Lys751Gln homozygous variant genotype in patients with EADC (OR = 0.24; 95% CI = 0.07–0.88), and for the XRCC1 Arg399Gln homozygous variant genotype in patients with BE (OR = 0.38; 95% CI = 0.12–0.64) and GERD (OR = 0.29; 95% CI = 0.12–0.66). We conclude that the malignant phenotype probably results from a summation of polymorphic nucleotide excision repair genes showing opposing effects (an increased risk of XPC versus a protective effect of XPD). The protective effect of the homozygous variant of XRCC1 Arg399Gln for GERD and BE suggests that base excision repair alterations may occur early in progression to EADC, likely in response to GERD-induced endogenous oxidative or inflammatory DNA damage. As GERD and BE are highly prevalent in the general population, this protective effect may well explain why only a fraction of individuals with GERD and BE progress into invasive EADC.</description><identifier>ISSN: 0143-3334</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/bgi115</identifier><identifier>PMID: 15878910</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adenocarcinoma - genetics ; Adult ; Alcohol Drinking ; Barrett esophagus ; Barrett Esophagus - genetics ; base excision repair ; Base Sequence ; BER ; Biological and medical sciences ; Carcinogenesis, carcinogens and anticarcinogens ; Case-Control Studies ; confidence interval ; DNA Primers ; DNA Repair - genetics ; DNA-Binding Proteins - genetics ; EADC ; esophageal adenocarcinoma ; Esophageal Neoplasms - genetics ; Female ; gastroesophageal reflux disease ; GERD ; Humans ; Life Style ; Male ; Medical sciences ; microsatellite instability ; Middle Aged ; mismatch repair ; MMR ; MSI ; NER ; nucleotide excision repair ; odds ratio ; PAT ; PCR ; poly(AT) ; polymerase chain reaction ; Polymorphism, Genetic ; Reference Values ; Risk Factors ; Smoking ; Tumors ; X-ray Repair Cross Complementing Protein 1 ; X-ray repair cross-complementing genes ; xeroderma pigmentosum group genes ; XPG genes ; XRCC genes</subject><ispartof>Carcinogenesis (New York), 2005-09, Vol.26 (9), p.1536-1541</ispartof><rights>2005 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Sep 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c522t-5d8f8d6ddd8cde9e375053e1797ae1e35fcaccb848a9a65ec360d0965faf898b3</citedby><cites>FETCH-LOGICAL-c522t-5d8f8d6ddd8cde9e375053e1797ae1e35fcaccb848a9a65ec360d0965faf898b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17082150$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15878910$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Casson, Alan G.</creatorcontrib><creatorcontrib>Zheng, Zuoyu</creatorcontrib><creatorcontrib>Evans, Susan C.</creatorcontrib><creatorcontrib>Veugelers, Paul J.</creatorcontrib><creatorcontrib>Porter, Geoffrey A.</creatorcontrib><creatorcontrib>Guernsey, Duane L.</creatorcontrib><title>Polymorphisms in DNA repair genes in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>To test the hypothesis that aberrations of DNA repair contribute to susceptibility for the progression of gastroesophageal reflux disease (GERD) into Barrett esophagus (BE) and esophageal adenocarcinoma (EADC), we studied the frequency of polymorphisms of selected DNA repair genes in patients with GERD (n = 126), BE (n = 125) and EADC (n = 56) enrolled in a 2-year prospective case–control study. Controls comprised 95 strictly asymptomatic healthy individuals. Using genomic DNA extracted from blood samples, we identified wild-type and polymorphic variants of XPD (Arg156Arg and Lys751Gln), XRCC1 (Arg194Trp and Arg399Gln) and XRCC3 (Thr241Met), and the poly (AT) insertion/deletion of XPC (PAT). Allelic frequencies were compared between cases and controls using logistic regression to calculate age, gender, smoking and alcohol-adjusted odds ratios (OR) and 95% confidence intervals (CI). Patients with EADC demonstrated a significantly higher frequency of the XPC PAT homozygous variant genotype compared with asymptomatic controls (OR = 3.82; 95% CI = 1.05–13.93). Significantly reduced frequencies were seen for the XPD Lys751Gln homozygous variant genotype in patients with EADC (OR = 0.24; 95% CI = 0.07–0.88), and for the XRCC1 Arg399Gln homozygous variant genotype in patients with BE (OR = 0.38; 95% CI = 0.12–0.64) and GERD (OR = 0.29; 95% CI = 0.12–0.66). We conclude that the malignant phenotype probably results from a summation of polymorphic nucleotide excision repair genes showing opposing effects (an increased risk of XPC versus a protective effect of XPD). The protective effect of the homozygous variant of XRCC1 Arg399Gln for GERD and BE suggests that base excision repair alterations may occur early in progression to EADC, likely in response to GERD-induced endogenous oxidative or inflammatory DNA damage. As GERD and BE are highly prevalent in the general population, this protective effect may well explain why only a fraction of individuals with GERD and BE progress into invasive EADC.</description><subject>Adenocarcinoma - genetics</subject><subject>Adult</subject><subject>Alcohol Drinking</subject><subject>Barrett esophagus</subject><subject>Barrett Esophagus - genetics</subject><subject>base excision repair</subject><subject>Base Sequence</subject><subject>BER</subject><subject>Biological and medical sciences</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>Case-Control Studies</subject><subject>confidence interval</subject><subject>DNA Primers</subject><subject>DNA Repair - genetics</subject><subject>DNA-Binding Proteins - genetics</subject><subject>EADC</subject><subject>esophageal adenocarcinoma</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Female</subject><subject>gastroesophageal reflux disease</subject><subject>GERD</subject><subject>Humans</subject><subject>Life Style</subject><subject>Male</subject><subject>Medical sciences</subject><subject>microsatellite instability</subject><subject>Middle Aged</subject><subject>mismatch repair</subject><subject>MMR</subject><subject>MSI</subject><subject>NER</subject><subject>nucleotide excision repair</subject><subject>odds ratio</subject><subject>PAT</subject><subject>PCR</subject><subject>poly(AT)</subject><subject>polymerase chain reaction</subject><subject>Polymorphism, Genetic</subject><subject>Reference Values</subject><subject>Risk Factors</subject><subject>Smoking</subject><subject>Tumors</subject><subject>X-ray Repair Cross Complementing Protein 1</subject><subject>X-ray repair cross-complementing genes</subject><subject>xeroderma pigmentosum group genes</subject><subject>XPG genes</subject><subject>XRCC genes</subject><issn>0143-3334</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0EFrFTEQB_Agin2tHr1KEBQ9rE02m93kWFu1YqmFKoqXMC-ZvJd2d7Mmu2C_vWv34QNPA5kfM5M_Ic84e8uZFscWkg398XoTOJcPyIpXNStKrthDsmK8EoUQojoghznfMMZrIfVjcsClapTmbEX8VWzvupiGbchdpqGnZ5cnNOEAIdEN9nj_Nm6RdrFFO7WQ6ADjNt73QqbRU8xx2MIGoaWv30FKOI5vKDjs43Jc7OAJeeShzfh0V4_Itw_vv56eFxdfPn46PbkorCzLsZBOeeVq55yyDjWKRjIpkDe6AeQopLdg7VpVCjTUEq2omWO6lh680motjsirZe6Q4q8J82i6kC22LfQYp2xK1oiqKdUMX_wHb-KU-vk2U3ItVFNzOaNiQTbFnBN6M6TQQboznJm_6Zvlg2ZJf_bPd0OndYdur3dxz-DlDkC20PoEvQ157xqmSi7ZfnHII_7-14d0a-pmDsWc__hpSn15_f3q-rMR4g85iJ-H</recordid><startdate>20050901</startdate><enddate>20050901</enddate><creator>Casson, Alan G.</creator><creator>Zheng, Zuoyu</creator><creator>Evans, Susan C.</creator><creator>Veugelers, Paul J.</creator><creator>Porter, Geoffrey A.</creator><creator>Guernsey, Duane L.</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20050901</creationdate><title>Polymorphisms in DNA repair genes in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma</title><author>Casson, Alan G. ; Zheng, Zuoyu ; Evans, Susan C. ; Veugelers, Paul J. ; Porter, Geoffrey A. ; Guernsey, Duane L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c522t-5d8f8d6ddd8cde9e375053e1797ae1e35fcaccb848a9a65ec360d0965faf898b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adenocarcinoma - genetics</topic><topic>Adult</topic><topic>Alcohol Drinking</topic><topic>Barrett esophagus</topic><topic>Barrett Esophagus - genetics</topic><topic>base excision repair</topic><topic>Base Sequence</topic><topic>BER</topic><topic>Biological and medical sciences</topic><topic>Carcinogenesis, carcinogens and anticarcinogens</topic><topic>Case-Control Studies</topic><topic>confidence interval</topic><topic>DNA Primers</topic><topic>DNA Repair - genetics</topic><topic>DNA-Binding Proteins - genetics</topic><topic>EADC</topic><topic>esophageal adenocarcinoma</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Female</topic><topic>gastroesophageal reflux disease</topic><topic>GERD</topic><topic>Humans</topic><topic>Life Style</topic><topic>Male</topic><topic>Medical sciences</topic><topic>microsatellite instability</topic><topic>Middle Aged</topic><topic>mismatch repair</topic><topic>MMR</topic><topic>MSI</topic><topic>NER</topic><topic>nucleotide excision repair</topic><topic>odds ratio</topic><topic>PAT</topic><topic>PCR</topic><topic>poly(AT)</topic><topic>polymerase chain reaction</topic><topic>Polymorphism, Genetic</topic><topic>Reference Values</topic><topic>Risk Factors</topic><topic>Smoking</topic><topic>Tumors</topic><topic>X-ray Repair Cross Complementing Protein 1</topic><topic>X-ray repair cross-complementing genes</topic><topic>xeroderma pigmentosum group genes</topic><topic>XPG genes</topic><topic>XRCC genes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Casson, Alan G.</creatorcontrib><creatorcontrib>Zheng, Zuoyu</creatorcontrib><creatorcontrib>Evans, Susan C.</creatorcontrib><creatorcontrib>Veugelers, Paul J.</creatorcontrib><creatorcontrib>Porter, Geoffrey A.</creatorcontrib><creatorcontrib>Guernsey, Duane L.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Casson, Alan G.</au><au>Zheng, Zuoyu</au><au>Evans, Susan C.</au><au>Veugelers, Paul J.</au><au>Porter, Geoffrey A.</au><au>Guernsey, Duane L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Polymorphisms in DNA repair genes in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>2005-09-01</date><risdate>2005</risdate><volume>26</volume><issue>9</issue><spage>1536</spage><epage>1541</epage><pages>1536-1541</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract>To test the hypothesis that aberrations of DNA repair contribute to susceptibility for the progression of gastroesophageal reflux disease (GERD) into Barrett esophagus (BE) and esophageal adenocarcinoma (EADC), we studied the frequency of polymorphisms of selected DNA repair genes in patients with GERD (n = 126), BE (n = 125) and EADC (n = 56) enrolled in a 2-year prospective case–control study. Controls comprised 95 strictly asymptomatic healthy individuals. Using genomic DNA extracted from blood samples, we identified wild-type and polymorphic variants of XPD (Arg156Arg and Lys751Gln), XRCC1 (Arg194Trp and Arg399Gln) and XRCC3 (Thr241Met), and the poly (AT) insertion/deletion of XPC (PAT). Allelic frequencies were compared between cases and controls using logistic regression to calculate age, gender, smoking and alcohol-adjusted odds ratios (OR) and 95% confidence intervals (CI). Patients with EADC demonstrated a significantly higher frequency of the XPC PAT homozygous variant genotype compared with asymptomatic controls (OR = 3.82; 95% CI = 1.05–13.93). Significantly reduced frequencies were seen for the XPD Lys751Gln homozygous variant genotype in patients with EADC (OR = 0.24; 95% CI = 0.07–0.88), and for the XRCC1 Arg399Gln homozygous variant genotype in patients with BE (OR = 0.38; 95% CI = 0.12–0.64) and GERD (OR = 0.29; 95% CI = 0.12–0.66). We conclude that the malignant phenotype probably results from a summation of polymorphic nucleotide excision repair genes showing opposing effects (an increased risk of XPC versus a protective effect of XPD). The protective effect of the homozygous variant of XRCC1 Arg399Gln for GERD and BE suggests that base excision repair alterations may occur early in progression to EADC, likely in response to GERD-induced endogenous oxidative or inflammatory DNA damage. As GERD and BE are highly prevalent in the general population, this protective effect may well explain why only a fraction of individuals with GERD and BE progress into invasive EADC.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>15878910</pmid><doi>10.1093/carcin/bgi115</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma - genetics Adult Alcohol Drinking Barrett esophagus Barrett Esophagus - genetics base excision repair Base Sequence BER Biological and medical sciences Carcinogenesis, carcinogens and anticarcinogens Case-Control Studies confidence interval DNA Primers DNA Repair - genetics DNA-Binding Proteins - genetics EADC esophageal adenocarcinoma Esophageal Neoplasms - genetics Female gastroesophageal reflux disease GERD Humans Life Style Male Medical sciences microsatellite instability Middle Aged mismatch repair MMR MSI NER nucleotide excision repair odds ratio PAT PCR poly(AT) polymerase chain reaction Polymorphism, Genetic Reference Values Risk Factors Smoking Tumors X-ray Repair Cross Complementing Protein 1 X-ray repair cross-complementing genes xeroderma pigmentosum group genes XPG genes XRCC genes |
| title | Polymorphisms in DNA repair genes in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma |
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