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Relevance of GSTM1, GSTT1, and GSTP1 gene polymorphisms to gastric cancer susceptibility and phenotype
Human glutathione S-transferases (GSTs) are phase II metabolizing enzymes that play a key role in protecting against cancer by detoxifying numerous potentially cytotoxic/genotoxic compounds. The genes encoding the human GST isoenzymes GSTM(mu)1, GSTT(theta)1 and GSTP(pi)1 harbour polymorphisms, whic...
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Published in: | Mutagenesis 2012-11, Vol.27 (6), p.771-777 |
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creator | GARCIA-GONZALEZ, Maasuncion QUINTERO, Enrique PEREZ-AISA, Maangeles MENDEZ-SANCHEZ, Isabel Ma THOMSON, Concha CARRERA, Patricia PIAZUELO, Elena JIMENEZ, Pilar ESPINEL, Jesús CAMPO, Rafael MANZANO, Marisa GEIJO, Fernando BUJANDA, Luis PELLISE, Maria GONZALEZ-HUIX, Ferrán ESPINOS, Jorge TITO, Llusia ZABALLA, Manuel PAZO, Roberto LANAS, Angel NICOLAS, David BENITO, Rafael STRUNK, Mark SANTOLARIA, Santos SOPENA, Federico BADIA, Maria HIJONA, Elizabeth |
description | Human glutathione S-transferases (GSTs) are phase II metabolizing enzymes that play a key role in protecting against cancer by detoxifying numerous potentially cytotoxic/genotoxic compounds. The genes encoding the human GST isoenzymes GSTM(mu)1, GSTT(theta)1 and GSTP(pi)1 harbour polymorphisms, which have been considered important modifiers of the individual risk for environmentally induced cancers such as gastric cancer (GC). However, results are inconsistent among studies from different geographic areas and ethnic groups. Our goal was to perform a nationwide, case-control study in Spain to evaluate the relevance of several functional GST gene polymorphisms and environmental factors to GC risk and phenotype. DNA from 557 GC patients and 557 sex- and age-matched healthy controls (HC) was typed for two deletions in the GSTM1 and GSTT1 genes and two SNPs in the GSTP1 gene (rs1695 and rs1138272) using polymerase chain reaction-restriction fragment length polymorphism methods. Logistic regression analysis identified Helicobacter pylori infection with CagA strains [odds ratio (OR): 2.36; 95% confidence interval (CI): 1.78-3.15], smoking habit (OR: 2.10; 95% CI: 1.48-2.97) and family history of GC (OR: 3.2; 95% CI: 2.02-5.16) as independent risk factors for GC. No differences in the frequencies of GSTM1 or GSTT1 null genotypes were observed between cases and controls (GSTM1: 50.8% vs. 48%; GSTT1: 21.5% vs. 21%). Moreover, simultaneous carriage of both, the GSTM1 and the GSTT1 null genotypes, was almost identical in both groups (10.7% in GC vs. 10.6% in HC). In addition, no significant differences in GSTP1 Ile105Val (rs1695) and GSTP1 Val114Ala (rs1138272) genotype distribution were observed between GC patients and controls. Subgroup analysis for age, gender, Helicobacter pylori status, smoking habits, family history of GC, anatomic location and histological subtype revealed no significant association between GST variants and GC risk. Our results show that the GST polymorphisms evaluated in this study are not relevant when determining the individual susceptibility to GC or phenotype in a South-European population. |
doi_str_mv | 10.1093/mutage/ges049 |
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The genes encoding the human GST isoenzymes GSTM(mu)1, GSTT(theta)1 and GSTP(pi)1 harbour polymorphisms, which have been considered important modifiers of the individual risk for environmentally induced cancers such as gastric cancer (GC). However, results are inconsistent among studies from different geographic areas and ethnic groups. Our goal was to perform a nationwide, case-control study in Spain to evaluate the relevance of several functional GST gene polymorphisms and environmental factors to GC risk and phenotype. DNA from 557 GC patients and 557 sex- and age-matched healthy controls (HC) was typed for two deletions in the GSTM1 and GSTT1 genes and two SNPs in the GSTP1 gene (rs1695 and rs1138272) using polymerase chain reaction-restriction fragment length polymorphism methods. Logistic regression analysis identified Helicobacter pylori infection with CagA strains [odds ratio (OR): 2.36; 95% confidence interval (CI): 1.78-3.15], smoking habit (OR: 2.10; 95% CI: 1.48-2.97) and family history of GC (OR: 3.2; 95% CI: 2.02-5.16) as independent risk factors for GC. No differences in the frequencies of GSTM1 or GSTT1 null genotypes were observed between cases and controls (GSTM1: 50.8% vs. 48%; GSTT1: 21.5% vs. 21%). Moreover, simultaneous carriage of both, the GSTM1 and the GSTT1 null genotypes, was almost identical in both groups (10.7% in GC vs. 10.6% in HC). In addition, no significant differences in GSTP1 Ile105Val (rs1695) and GSTP1 Val114Ala (rs1138272) genotype distribution were observed between GC patients and controls. Subgroup analysis for age, gender, Helicobacter pylori status, smoking habits, family history of GC, anatomic location and histological subtype revealed no significant association between GST variants and GC risk. Our results show that the GST polymorphisms evaluated in this study are not relevant when determining the individual susceptibility to GC or phenotype in a South-European population.</description><identifier>ISSN: 0267-8357</identifier><identifier>EISSN: 1464-3804</identifier><identifier>DOI: 10.1093/mutage/ges049</identifier><identifier>PMID: 22952149</identifier><identifier>CODEN: MUTAEX</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Biological and medical sciences ; Case-Control Studies ; Female ; Fundamental and applied biological sciences. Psychology ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Glutathione S-Transferase pi - genetics ; Glutathione S-Transferase pi - metabolism ; Glutathione Transferase - genetics ; Glutathione Transferase - metabolism ; Helicobacter Infections - complications ; Helicobacter pylori - pathogenicity ; Humans ; Isoenzymes ; Logistic Models ; Male ; Middle Aged ; Molecular and cellular biology ; Molecular genetics ; Mutagenesis. Repair ; Odds Ratio ; Phenotype ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Polymorphism, Single Nucleotide ; Risk Factors ; Smoking - adverse effects ; Spain - epidemiology ; Stomach Neoplasms - enzymology ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology</subject><ispartof>Mutagenesis, 2012-11, Vol.27 (6), p.771-777</ispartof><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-982bf82f8832cc4f10faf99f7dff167297872c3140891502f7a8891097c2c4943</citedby><cites>FETCH-LOGICAL-c362t-982bf82f8832cc4f10faf99f7dff167297872c3140891502f7a8891097c2c4943</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26592925$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22952149$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GARCIA-GONZALEZ, Maasuncion</creatorcontrib><creatorcontrib>QUINTERO, Enrique</creatorcontrib><creatorcontrib>PEREZ-AISA, Maangeles</creatorcontrib><creatorcontrib>MENDEZ-SANCHEZ, Isabel Ma</creatorcontrib><creatorcontrib>THOMSON, Concha</creatorcontrib><creatorcontrib>CARRERA, Patricia</creatorcontrib><creatorcontrib>PIAZUELO, Elena</creatorcontrib><creatorcontrib>JIMENEZ, Pilar</creatorcontrib><creatorcontrib>ESPINEL, Jesús</creatorcontrib><creatorcontrib>CAMPO, Rafael</creatorcontrib><creatorcontrib>MANZANO, Marisa</creatorcontrib><creatorcontrib>GEIJO, Fernando</creatorcontrib><creatorcontrib>BUJANDA, Luis</creatorcontrib><creatorcontrib>PELLISE, Maria</creatorcontrib><creatorcontrib>GONZALEZ-HUIX, Ferrán</creatorcontrib><creatorcontrib>ESPINOS, Jorge</creatorcontrib><creatorcontrib>TITO, Llusia</creatorcontrib><creatorcontrib>ZABALLA, Manuel</creatorcontrib><creatorcontrib>PAZO, Roberto</creatorcontrib><creatorcontrib>LANAS, Angel</creatorcontrib><creatorcontrib>NICOLAS, David</creatorcontrib><creatorcontrib>BENITO, Rafael</creatorcontrib><creatorcontrib>STRUNK, Mark</creatorcontrib><creatorcontrib>SANTOLARIA, Santos</creatorcontrib><creatorcontrib>SOPENA, Federico</creatorcontrib><creatorcontrib>BADIA, Maria</creatorcontrib><creatorcontrib>HIJONA, Elizabeth</creatorcontrib><title>Relevance of GSTM1, GSTT1, and GSTP1 gene polymorphisms to gastric cancer susceptibility and phenotype</title><title>Mutagenesis</title><addtitle>Mutagenesis</addtitle><description>Human glutathione S-transferases (GSTs) are phase II metabolizing enzymes that play a key role in protecting against cancer by detoxifying numerous potentially cytotoxic/genotoxic compounds. The genes encoding the human GST isoenzymes GSTM(mu)1, GSTT(theta)1 and GSTP(pi)1 harbour polymorphisms, which have been considered important modifiers of the individual risk for environmentally induced cancers such as gastric cancer (GC). However, results are inconsistent among studies from different geographic areas and ethnic groups. Our goal was to perform a nationwide, case-control study in Spain to evaluate the relevance of several functional GST gene polymorphisms and environmental factors to GC risk and phenotype. DNA from 557 GC patients and 557 sex- and age-matched healthy controls (HC) was typed for two deletions in the GSTM1 and GSTT1 genes and two SNPs in the GSTP1 gene (rs1695 and rs1138272) using polymerase chain reaction-restriction fragment length polymorphism methods. Logistic regression analysis identified Helicobacter pylori infection with CagA strains [odds ratio (OR): 2.36; 95% confidence interval (CI): 1.78-3.15], smoking habit (OR: 2.10; 95% CI: 1.48-2.97) and family history of GC (OR: 3.2; 95% CI: 2.02-5.16) as independent risk factors for GC. No differences in the frequencies of GSTM1 or GSTT1 null genotypes were observed between cases and controls (GSTM1: 50.8% vs. 48%; GSTT1: 21.5% vs. 21%). Moreover, simultaneous carriage of both, the GSTM1 and the GSTT1 null genotypes, was almost identical in both groups (10.7% in GC vs. 10.6% in HC). In addition, no significant differences in GSTP1 Ile105Val (rs1695) and GSTP1 Val114Ala (rs1138272) genotype distribution were observed between GC patients and controls. Subgroup analysis for age, gender, Helicobacter pylori status, smoking habits, family history of GC, anatomic location and histological subtype revealed no significant association between GST variants and GC risk. Our results show that the GST polymorphisms evaluated in this study are not relevant when determining the individual susceptibility to GC or phenotype in a South-European population.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Frequency</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Glutathione S-Transferase pi - genetics</subject><subject>Glutathione S-Transferase pi - metabolism</subject><subject>Glutathione Transferase - genetics</subject><subject>Glutathione Transferase - metabolism</subject><subject>Helicobacter Infections - complications</subject><subject>Helicobacter pylori - pathogenicity</subject><subject>Humans</subject><subject>Isoenzymes</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Mutagenesis. Repair</subject><subject>Odds Ratio</subject><subject>Phenotype</subject><subject>Polymerase Chain Reaction</subject><subject>Polymorphism, Restriction Fragment Length</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Risk Factors</subject><subject>Smoking - adverse effects</subject><subject>Spain - epidemiology</subject><subject>Stomach Neoplasms - enzymology</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - pathology</subject><issn>0267-8357</issn><issn>1464-3804</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNpFkDFPwzAQRi0EoqUwsqIsSAyE2hcntkdUQUEqAkGZI9e106AkDnaClH9PQgos993wvtPpIXRO8A3BIpqXbSMzPc-0x1QcoCmhCQ0jjukhmmJIWMijmE3QifcfGBMGCT5GEwARA6FiisyrLvSXrJQOrAmWb-sncj3Eug9ZbYf1hQSZrnRQ26Irrat3uS990Nggk75xuQrUUHeBb73SdZNv8iJvup92vdOVbbpan6IjIwuvz_Y5Q-_3d-vFQ7h6Xj4ublehihJoQsFhYzgYziNQihqCjTRCGLY1hiQMBOMMVEQo5oLEGAyTvN-wYAoUFTSaoavxbu3sZ6t9k5Z5_1VRyErb1qeEQJJAP3CPhiOqnPXeaZPWLi-l61KC00FtOqpNR7U9f7E_3W5Kvf2jf132wOUekF7JwrheS-7_uSQWICCOvgFFVoII</recordid><startdate>20121101</startdate><enddate>20121101</enddate><creator>GARCIA-GONZALEZ, Maasuncion</creator><creator>QUINTERO, Enrique</creator><creator>PEREZ-AISA, Maangeles</creator><creator>MENDEZ-SANCHEZ, Isabel Ma</creator><creator>THOMSON, Concha</creator><creator>CARRERA, Patricia</creator><creator>PIAZUELO, Elena</creator><creator>JIMENEZ, Pilar</creator><creator>ESPINEL, Jesús</creator><creator>CAMPO, Rafael</creator><creator>MANZANO, Marisa</creator><creator>GEIJO, Fernando</creator><creator>BUJANDA, Luis</creator><creator>PELLISE, Maria</creator><creator>GONZALEZ-HUIX, Ferrán</creator><creator>ESPINOS, Jorge</creator><creator>TITO, Llusia</creator><creator>ZABALLA, Manuel</creator><creator>PAZO, Roberto</creator><creator>LANAS, Angel</creator><creator>NICOLAS, David</creator><creator>BENITO, Rafael</creator><creator>STRUNK, Mark</creator><creator>SANTOLARIA, Santos</creator><creator>SOPENA, Federico</creator><creator>BADIA, Maria</creator><creator>HIJONA, Elizabeth</creator><general>Oxford University Press</general><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>7X8</scope></search><sort><creationdate>20121101</creationdate><title>Relevance of GSTM1, GSTT1, and GSTP1 gene polymorphisms to gastric cancer susceptibility and phenotype</title><author>GARCIA-GONZALEZ, Maasuncion ; QUINTERO, Enrique ; PEREZ-AISA, Maangeles ; MENDEZ-SANCHEZ, Isabel Ma ; THOMSON, Concha ; CARRERA, Patricia ; PIAZUELO, Elena ; JIMENEZ, Pilar ; ESPINEL, Jesús ; CAMPO, Rafael ; MANZANO, Marisa ; GEIJO, Fernando ; BUJANDA, Luis ; PELLISE, Maria ; GONZALEZ-HUIX, Ferrán ; ESPINOS, Jorge ; TITO, Llusia ; ZABALLA, Manuel ; PAZO, Roberto ; LANAS, Angel ; NICOLAS, David ; BENITO, Rafael ; STRUNK, Mark ; SANTOLARIA, Santos ; SOPENA, Federico ; BADIA, Maria ; HIJONA, Elizabeth</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-982bf82f8832cc4f10faf99f7dff167297872c3140891502f7a8891097c2c4943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Frequency</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Glutathione S-Transferase pi - genetics</topic><topic>Glutathione S-Transferase pi - metabolism</topic><topic>Glutathione Transferase - genetics</topic><topic>Glutathione Transferase - metabolism</topic><topic>Helicobacter Infections - complications</topic><topic>Helicobacter pylori - pathogenicity</topic><topic>Humans</topic><topic>Isoenzymes</topic><topic>Logistic Models</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Mutagenesis. Repair</topic><topic>Odds Ratio</topic><topic>Phenotype</topic><topic>Polymerase Chain Reaction</topic><topic>Polymorphism, Restriction Fragment Length</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Risk Factors</topic><topic>Smoking - adverse effects</topic><topic>Spain - epidemiology</topic><topic>Stomach Neoplasms - enzymology</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GARCIA-GONZALEZ, Maasuncion</creatorcontrib><creatorcontrib>QUINTERO, Enrique</creatorcontrib><creatorcontrib>PEREZ-AISA, Maangeles</creatorcontrib><creatorcontrib>MENDEZ-SANCHEZ, Isabel Ma</creatorcontrib><creatorcontrib>THOMSON, Concha</creatorcontrib><creatorcontrib>CARRERA, Patricia</creatorcontrib><creatorcontrib>PIAZUELO, Elena</creatorcontrib><creatorcontrib>JIMENEZ, Pilar</creatorcontrib><creatorcontrib>ESPINEL, Jesús</creatorcontrib><creatorcontrib>CAMPO, Rafael</creatorcontrib><creatorcontrib>MANZANO, Marisa</creatorcontrib><creatorcontrib>GEIJO, Fernando</creatorcontrib><creatorcontrib>BUJANDA, Luis</creatorcontrib><creatorcontrib>PELLISE, Maria</creatorcontrib><creatorcontrib>GONZALEZ-HUIX, Ferrán</creatorcontrib><creatorcontrib>ESPINOS, Jorge</creatorcontrib><creatorcontrib>TITO, Llusia</creatorcontrib><creatorcontrib>ZABALLA, Manuel</creatorcontrib><creatorcontrib>PAZO, Roberto</creatorcontrib><creatorcontrib>LANAS, Angel</creatorcontrib><creatorcontrib>NICOLAS, David</creatorcontrib><creatorcontrib>BENITO, Rafael</creatorcontrib><creatorcontrib>STRUNK, Mark</creatorcontrib><creatorcontrib>SANTOLARIA, Santos</creatorcontrib><creatorcontrib>SOPENA, Federico</creatorcontrib><creatorcontrib>BADIA, Maria</creatorcontrib><creatorcontrib>HIJONA, Elizabeth</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>Mutagenesis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GARCIA-GONZALEZ, Maasuncion</au><au>QUINTERO, Enrique</au><au>PEREZ-AISA, Maangeles</au><au>MENDEZ-SANCHEZ, Isabel Ma</au><au>THOMSON, Concha</au><au>CARRERA, Patricia</au><au>PIAZUELO, Elena</au><au>JIMENEZ, Pilar</au><au>ESPINEL, Jesús</au><au>CAMPO, Rafael</au><au>MANZANO, Marisa</au><au>GEIJO, Fernando</au><au>BUJANDA, Luis</au><au>PELLISE, Maria</au><au>GONZALEZ-HUIX, Ferrán</au><au>ESPINOS, Jorge</au><au>TITO, Llusia</au><au>ZABALLA, Manuel</au><au>PAZO, Roberto</au><au>LANAS, Angel</au><au>NICOLAS, David</au><au>BENITO, Rafael</au><au>STRUNK, Mark</au><au>SANTOLARIA, Santos</au><au>SOPENA, Federico</au><au>BADIA, Maria</au><au>HIJONA, Elizabeth</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Relevance of GSTM1, GSTT1, and GSTP1 gene polymorphisms to gastric cancer susceptibility and phenotype</atitle><jtitle>Mutagenesis</jtitle><addtitle>Mutagenesis</addtitle><date>2012-11-01</date><risdate>2012</risdate><volume>27</volume><issue>6</issue><spage>771</spage><epage>777</epage><pages>771-777</pages><issn>0267-8357</issn><eissn>1464-3804</eissn><coden>MUTAEX</coden><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Human glutathione S-transferases (GSTs) are phase II metabolizing enzymes that play a key role in protecting against cancer by detoxifying numerous potentially cytotoxic/genotoxic compounds. The genes encoding the human GST isoenzymes GSTM(mu)1, GSTT(theta)1 and GSTP(pi)1 harbour polymorphisms, which have been considered important modifiers of the individual risk for environmentally induced cancers such as gastric cancer (GC). However, results are inconsistent among studies from different geographic areas and ethnic groups. Our goal was to perform a nationwide, case-control study in Spain to evaluate the relevance of several functional GST gene polymorphisms and environmental factors to GC risk and phenotype. DNA from 557 GC patients and 557 sex- and age-matched healthy controls (HC) was typed for two deletions in the GSTM1 and GSTT1 genes and two SNPs in the GSTP1 gene (rs1695 and rs1138272) using polymerase chain reaction-restriction fragment length polymorphism methods. Logistic regression analysis identified Helicobacter pylori infection with CagA strains [odds ratio (OR): 2.36; 95% confidence interval (CI): 1.78-3.15], smoking habit (OR: 2.10; 95% CI: 1.48-2.97) and family history of GC (OR: 3.2; 95% CI: 2.02-5.16) as independent risk factors for GC. No differences in the frequencies of GSTM1 or GSTT1 null genotypes were observed between cases and controls (GSTM1: 50.8% vs. 48%; GSTT1: 21.5% vs. 21%). Moreover, simultaneous carriage of both, the GSTM1 and the GSTT1 null genotypes, was almost identical in both groups (10.7% in GC vs. 10.6% in HC). In addition, no significant differences in GSTP1 Ile105Val (rs1695) and GSTP1 Val114Ala (rs1138272) genotype distribution were observed between GC patients and controls. Subgroup analysis for age, gender, Helicobacter pylori status, smoking habits, family history of GC, anatomic location and histological subtype revealed no significant association between GST variants and GC risk. Our results show that the GST polymorphisms evaluated in this study are not relevant when determining the individual susceptibility to GC or phenotype in a South-European population.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>22952149</pmid><doi>10.1093/mutage/ges049</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Aged Aged, 80 and over Biological and medical sciences Case-Control Studies Female Fundamental and applied biological sciences. Psychology Gene Frequency Genetic Predisposition to Disease Genotype Glutathione S-Transferase pi - genetics Glutathione S-Transferase pi - metabolism Glutathione Transferase - genetics Glutathione Transferase - metabolism Helicobacter Infections - complications Helicobacter pylori - pathogenicity Humans Isoenzymes Logistic Models Male Middle Aged Molecular and cellular biology Molecular genetics Mutagenesis. Repair Odds Ratio Phenotype Polymerase Chain Reaction Polymorphism, Restriction Fragment Length Polymorphism, Single Nucleotide Risk Factors Smoking - adverse effects Spain - epidemiology Stomach Neoplasms - enzymology Stomach Neoplasms - genetics Stomach Neoplasms - pathology |
title | Relevance of GSTM1, GSTT1, and GSTP1 gene polymorphisms to gastric cancer susceptibility and phenotype |
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