Possible gene dosage effect of glutathione-S-transferases on atopic asthma: Using real-time PCR for quantification of GSTM1 and GSTT1 gene copy numbers
Asthma is a complex genetic disorder characterized by chronic inflammation in the airways. As oxidative stress is a key component of inflammation, variations in genes involved in antioxidant defense could therefore be likely candidates for asthma. Three enzymes from the superfamily glutathione‐S‐tra...
Gespeichert in:
| Veröffentlicht in: | Human mutation 2004-09, Vol.24 (3), p.208-214 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 214 |
|---|---|
| container_issue | 3 |
| container_start_page | 208 |
| container_title | Human mutation |
| container_volume | 24 |
| creator | Brasch-Andersen, Charlotte Christiansen, Lene Tan, Qihua Haagerup, Annette Vestbo, Jørgen Kruse, Torben A. |
| description | Asthma is a complex genetic disorder characterized by chronic inflammation in the airways. As oxidative stress is a key component of inflammation, variations in genes involved in antioxidant defense could therefore be likely candidates for asthma. Three enzymes from the superfamily glutathione‐S‐transferase (GST) involved in the antioxidant defense were tested for association to asthma using 246 Danish atopic families in a family‐based transmission disequilibrium test (TDT) design. A real‐time PCR assay for relative quantification of gene copy number of GSTM1 and GSTT1 was developed. The assay made it possible to distinguish individuals with zero, one, and two copies and thereby to investigate whether the GST genes influenced susceptibility to asthma in a dose‐dependent manner. We found that asthmatic patients with two copies of GSTM1 were significantly underrepresented (p |
| doi_str_mv | 10.1002/humu.20074 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_66772849</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>781202151</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4574-bf0046d43ce6f55b2d28145dd45087f1625b2bf952151d00f4ee0b4f69d4210d3</originalsourceid><addsrcrecordid>eNqFkcGO0zAURSMEYoaBDR-ALBYskDLYjh0n7FAFHaQOVEwrlpaTPLceErtjO4J-Cb-LQwpILGDlK-u8Yz3fLHtK8CXBmL7aj8N4STEW7F52TnBd5ema3Z8yr3MhanaWPQrhFmNccV48zM4IL1Jm1Xn2fe1CME0PaAcWUOeC2gECraGNyGm068eo4t44C_lNHr2yQYNXAQJyFqnoDqZFKsT9oF6jbTB2hzyoPo9mALRefELaeXQ3KhuNNq2KSTRplzeba4KU7aa0IfPjrTsckR2HBnx4nD3Qqg_w5HReZNt3bzeLq3z1cfl-8WaVt4wLljc6bVp2rGih1Jw3tKMVYbzrGMeV0KSk6a7RNaeEkw5jzQBww3RZd4wS3BUX2YvZe_DuboQQ5WBCC32vLLgxyLIUglas_i9IKsyLkooEPv8LvHWjt2kJSWpBBSvLIkEvZ6j16f89aHnwZlD-KAmWU6lyKlX-LDXBz07GsRmg-4OeWkwAmYGvpofjP1Tyanu9_SXN5xkTInz7PaP8F1mKQnD5-cMypUpsNuu1XBU_AJN0u2I</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>197274663</pqid></control><display><type>article</type><title>Possible gene dosage effect of glutathione-S-transferases on atopic asthma: Using real-time PCR for quantification of GSTM1 and GSTT1 gene copy numbers</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Brasch-Andersen, Charlotte ; Christiansen, Lene ; Tan, Qihua ; Haagerup, Annette ; Vestbo, Jørgen ; Kruse, Torben A.</creator><creatorcontrib>Brasch-Andersen, Charlotte ; Christiansen, Lene ; Tan, Qihua ; Haagerup, Annette ; Vestbo, Jørgen ; Kruse, Torben A.</creatorcontrib><description>Asthma is a complex genetic disorder characterized by chronic inflammation in the airways. As oxidative stress is a key component of inflammation, variations in genes involved in antioxidant defense could therefore be likely candidates for asthma. Three enzymes from the superfamily glutathione‐S‐transferase (GST) involved in the antioxidant defense were tested for association to asthma using 246 Danish atopic families in a family‐based transmission disequilibrium test (TDT) design. A real‐time PCR assay for relative quantification of gene copy number of GSTM1 and GSTT1 was developed. The assay made it possible to distinguish individuals with zero, one, and two copies and thereby to investigate whether the GST genes influenced susceptibility to asthma in a dose‐dependent manner. We found that asthmatic patients with two copies of GSTM1 were significantly underrepresented (p<0.0005) and the significance increased by 10‐fold when only atopic asthmatics were analyzed (p<0.00005). GSTT1 was significantly associated in an additive model to asthma, in which the alleles carrying the deletion of the gene were transmitted to affected offspring more often than expected by chance (p=0.019). The same transmission disequilibrium of the null GSTT1 allele was seen in patients with atopic asthma (p=0.021). The polymorphism c.342A>G (p.I105V) in GSTP1 has previously been suggested as a risk factor for asthma. However, significant association with asthma or related atopic phenotypes could not be established in our study. We conclude that deletions of GSTM1 and GSTT1 could be risk factors for asthma and that the genes might have a protective role in the development of atopic asthma. Hum Mutat 24:208–214, 2004. © 2004 Wiley‐Liss, Inc.</description><identifier>ISSN: 1059-7794</identifier><identifier>EISSN: 1098-1004</identifier><identifier>DOI: 10.1002/humu.20074</identifier><identifier>PMID: 15300848</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Alleles ; Asthma ; Asthma - epidemiology ; Asthma - genetics ; Asthma - immunology ; atopy ; Biochemistry ; Child ; Computer Systems ; Denmark - epidemiology ; Enzymes ; Gene Dosage ; Genes ; Genes, Recessive ; Genetic Heterogeneity ; Genetic Predisposition to Disease ; Genetics ; Genotype ; Glutathione Transferase - genetics ; Glutathione Transferase - physiology ; glutathione-S-transferase M1 ; glutathione-S-transferase P1 ; glutathione-S-transferase T1 ; Health care ; Hospitals ; Humans ; Hypersensitivity, Immediate - epidemiology ; Hypersensitivity, Immediate - genetics ; Hypersensitivity, Immediate - immunology ; Inflammation ; Oxidative stress ; Phenotype ; Polymerase Chain Reaction - methods ; Polymorphism ; Polymorphism, Single Nucleotide ; real-time PCR quantification ; Risk factors ; Sequence Deletion ; transmission disequilibrium test</subject><ispartof>Human mutation, 2004-09, Vol.24 (3), p.208-214</ispartof><rights>Copyright © 2004 Wiley‐Liss, Inc.</rights><rights>Copyright 2004 Wiley-Liss, Inc.</rights><rights>Copyright © 2004 Wiley-Liss, Inc., A Wiley Company</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4574-bf0046d43ce6f55b2d28145dd45087f1625b2bf952151d00f4ee0b4f69d4210d3</citedby><cites>FETCH-LOGICAL-c4574-bf0046d43ce6f55b2d28145dd45087f1625b2bf952151d00f4ee0b4f69d4210d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fhumu.20074$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fhumu.20074$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15300848$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brasch-Andersen, Charlotte</creatorcontrib><creatorcontrib>Christiansen, Lene</creatorcontrib><creatorcontrib>Tan, Qihua</creatorcontrib><creatorcontrib>Haagerup, Annette</creatorcontrib><creatorcontrib>Vestbo, Jørgen</creatorcontrib><creatorcontrib>Kruse, Torben A.</creatorcontrib><title>Possible gene dosage effect of glutathione-S-transferases on atopic asthma: Using real-time PCR for quantification of GSTM1 and GSTT1 gene copy numbers</title><title>Human mutation</title><addtitle>Hum. Mutat</addtitle><description>Asthma is a complex genetic disorder characterized by chronic inflammation in the airways. As oxidative stress is a key component of inflammation, variations in genes involved in antioxidant defense could therefore be likely candidates for asthma. Three enzymes from the superfamily glutathione‐S‐transferase (GST) involved in the antioxidant defense were tested for association to asthma using 246 Danish atopic families in a family‐based transmission disequilibrium test (TDT) design. A real‐time PCR assay for relative quantification of gene copy number of GSTM1 and GSTT1 was developed. The assay made it possible to distinguish individuals with zero, one, and two copies and thereby to investigate whether the GST genes influenced susceptibility to asthma in a dose‐dependent manner. We found that asthmatic patients with two copies of GSTM1 were significantly underrepresented (p<0.0005) and the significance increased by 10‐fold when only atopic asthmatics were analyzed (p<0.00005). GSTT1 was significantly associated in an additive model to asthma, in which the alleles carrying the deletion of the gene were transmitted to affected offspring more often than expected by chance (p=0.019). The same transmission disequilibrium of the null GSTT1 allele was seen in patients with atopic asthma (p=0.021). The polymorphism c.342A>G (p.I105V) in GSTP1 has previously been suggested as a risk factor for asthma. However, significant association with asthma or related atopic phenotypes could not be established in our study. We conclude that deletions of GSTM1 and GSTT1 could be risk factors for asthma and that the genes might have a protective role in the development of atopic asthma. Hum Mutat 24:208–214, 2004. © 2004 Wiley‐Liss, Inc.</description><subject>Alleles</subject><subject>Asthma</subject><subject>Asthma - epidemiology</subject><subject>Asthma - genetics</subject><subject>Asthma - immunology</subject><subject>atopy</subject><subject>Biochemistry</subject><subject>Child</subject><subject>Computer Systems</subject><subject>Denmark - epidemiology</subject><subject>Enzymes</subject><subject>Gene Dosage</subject><subject>Genes</subject><subject>Genes, Recessive</subject><subject>Genetic Heterogeneity</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetics</subject><subject>Genotype</subject><subject>Glutathione Transferase - genetics</subject><subject>Glutathione Transferase - physiology</subject><subject>glutathione-S-transferase M1</subject><subject>glutathione-S-transferase P1</subject><subject>glutathione-S-transferase T1</subject><subject>Health care</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Hypersensitivity, Immediate - epidemiology</subject><subject>Hypersensitivity, Immediate - genetics</subject><subject>Hypersensitivity, Immediate - immunology</subject><subject>Inflammation</subject><subject>Oxidative stress</subject><subject>Phenotype</subject><subject>Polymerase Chain Reaction - methods</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>real-time PCR quantification</subject><subject>Risk factors</subject><subject>Sequence Deletion</subject><subject>transmission disequilibrium test</subject><issn>1059-7794</issn><issn>1098-1004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkcGO0zAURSMEYoaBDR-ALBYskDLYjh0n7FAFHaQOVEwrlpaTPLceErtjO4J-Cb-LQwpILGDlK-u8Yz3fLHtK8CXBmL7aj8N4STEW7F52TnBd5ema3Z8yr3MhanaWPQrhFmNccV48zM4IL1Jm1Xn2fe1CME0PaAcWUOeC2gECraGNyGm068eo4t44C_lNHr2yQYNXAQJyFqnoDqZFKsT9oF6jbTB2hzyoPo9mALRefELaeXQ3KhuNNq2KSTRplzeba4KU7aa0IfPjrTsckR2HBnx4nD3Qqg_w5HReZNt3bzeLq3z1cfl-8WaVt4wLljc6bVp2rGih1Jw3tKMVYbzrGMeV0KSk6a7RNaeEkw5jzQBww3RZd4wS3BUX2YvZe_DuboQQ5WBCC32vLLgxyLIUglas_i9IKsyLkooEPv8LvHWjt2kJSWpBBSvLIkEvZ6j16f89aHnwZlD-KAmWU6lyKlX-LDXBz07GsRmg-4OeWkwAmYGvpofjP1Tyanu9_SXN5xkTInz7PaP8F1mKQnD5-cMypUpsNuu1XBU_AJN0u2I</recordid><startdate>200409</startdate><enddate>200409</enddate><creator>Brasch-Andersen, Charlotte</creator><creator>Christiansen, Lene</creator><creator>Tan, Qihua</creator><creator>Haagerup, Annette</creator><creator>Vestbo, Jørgen</creator><creator>Kruse, Torben A.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Hindawi Limited</general><scope>BSCLL</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>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>200409</creationdate><title>Possible gene dosage effect of glutathione-S-transferases on atopic asthma: Using real-time PCR for quantification of GSTM1 and GSTT1 gene copy numbers</title><author>Brasch-Andersen, Charlotte ; Christiansen, Lene ; Tan, Qihua ; Haagerup, Annette ; Vestbo, Jørgen ; Kruse, Torben A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4574-bf0046d43ce6f55b2d28145dd45087f1625b2bf952151d00f4ee0b4f69d4210d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Alleles</topic><topic>Asthma</topic><topic>Asthma - epidemiology</topic><topic>Asthma - genetics</topic><topic>Asthma - immunology</topic><topic>atopy</topic><topic>Biochemistry</topic><topic>Child</topic><topic>Computer Systems</topic><topic>Denmark - epidemiology</topic><topic>Enzymes</topic><topic>Gene Dosage</topic><topic>Genes</topic><topic>Genes, Recessive</topic><topic>Genetic Heterogeneity</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetics</topic><topic>Genotype</topic><topic>Glutathione Transferase - genetics</topic><topic>Glutathione Transferase - physiology</topic><topic>glutathione-S-transferase M1</topic><topic>glutathione-S-transferase P1</topic><topic>glutathione-S-transferase T1</topic><topic>Health care</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Hypersensitivity, Immediate - epidemiology</topic><topic>Hypersensitivity, Immediate - genetics</topic><topic>Hypersensitivity, Immediate - immunology</topic><topic>Inflammation</topic><topic>Oxidative stress</topic><topic>Phenotype</topic><topic>Polymerase Chain Reaction - methods</topic><topic>Polymorphism</topic><topic>Polymorphism, Single Nucleotide</topic><topic>real-time PCR quantification</topic><topic>Risk factors</topic><topic>Sequence Deletion</topic><topic>transmission disequilibrium test</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brasch-Andersen, Charlotte</creatorcontrib><creatorcontrib>Christiansen, Lene</creatorcontrib><creatorcontrib>Tan, Qihua</creatorcontrib><creatorcontrib>Haagerup, Annette</creatorcontrib><creatorcontrib>Vestbo, Jørgen</creatorcontrib><creatorcontrib>Kruse, Torben A.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Human mutation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brasch-Andersen, Charlotte</au><au>Christiansen, Lene</au><au>Tan, Qihua</au><au>Haagerup, Annette</au><au>Vestbo, Jørgen</au><au>Kruse, Torben A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Possible gene dosage effect of glutathione-S-transferases on atopic asthma: Using real-time PCR for quantification of GSTM1 and GSTT1 gene copy numbers</atitle><jtitle>Human mutation</jtitle><addtitle>Hum. Mutat</addtitle><date>2004-09</date><risdate>2004</risdate><volume>24</volume><issue>3</issue><spage>208</spage><epage>214</epage><pages>208-214</pages><issn>1059-7794</issn><eissn>1098-1004</eissn><abstract>Asthma is a complex genetic disorder characterized by chronic inflammation in the airways. As oxidative stress is a key component of inflammation, variations in genes involved in antioxidant defense could therefore be likely candidates for asthma. Three enzymes from the superfamily glutathione‐S‐transferase (GST) involved in the antioxidant defense were tested for association to asthma using 246 Danish atopic families in a family‐based transmission disequilibrium test (TDT) design. A real‐time PCR assay for relative quantification of gene copy number of GSTM1 and GSTT1 was developed. The assay made it possible to distinguish individuals with zero, one, and two copies and thereby to investigate whether the GST genes influenced susceptibility to asthma in a dose‐dependent manner. We found that asthmatic patients with two copies of GSTM1 were significantly underrepresented (p<0.0005) and the significance increased by 10‐fold when only atopic asthmatics were analyzed (p<0.00005). GSTT1 was significantly associated in an additive model to asthma, in which the alleles carrying the deletion of the gene were transmitted to affected offspring more often than expected by chance (p=0.019). The same transmission disequilibrium of the null GSTT1 allele was seen in patients with atopic asthma (p=0.021). The polymorphism c.342A>G (p.I105V) in GSTP1 has previously been suggested as a risk factor for asthma. However, significant association with asthma or related atopic phenotypes could not be established in our study. We conclude that deletions of GSTM1 and GSTT1 could be risk factors for asthma and that the genes might have a protective role in the development of atopic asthma. Hum Mutat 24:208–214, 2004. © 2004 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>15300848</pmid><doi>10.1002/humu.20074</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1059-7794 |
| ispartof | Human mutation, 2004-09, Vol.24 (3), p.208-214 |
| issn | 1059-7794 1098-1004 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_66772849 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Alleles Asthma Asthma - epidemiology Asthma - genetics Asthma - immunology atopy Biochemistry Child Computer Systems Denmark - epidemiology Enzymes Gene Dosage Genes Genes, Recessive Genetic Heterogeneity Genetic Predisposition to Disease Genetics Genotype Glutathione Transferase - genetics Glutathione Transferase - physiology glutathione-S-transferase M1 glutathione-S-transferase P1 glutathione-S-transferase T1 Health care Hospitals Humans Hypersensitivity, Immediate - epidemiology Hypersensitivity, Immediate - genetics Hypersensitivity, Immediate - immunology Inflammation Oxidative stress Phenotype Polymerase Chain Reaction - methods Polymorphism Polymorphism, Single Nucleotide real-time PCR quantification Risk factors Sequence Deletion transmission disequilibrium test |
| title | Possible gene dosage effect of glutathione-S-transferases on atopic asthma: Using real-time PCR for quantification of GSTM1 and GSTT1 gene copy numbers |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T19%3A23%3A49IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Possible%20gene%20dosage%20effect%20of%20glutathione-S-transferases%20on%20atopic%20asthma:%20Using%20real-time%20PCR%20for%20quantification%20of%20GSTM1%20and%20GSTT1%20gene%20copy%20numbers&rft.jtitle=Human%20mutation&rft.au=Brasch-Andersen,%20Charlotte&rft.date=2004-09&rft.volume=24&rft.issue=3&rft.spage=208&rft.epage=214&rft.pages=208-214&rft.issn=1059-7794&rft.eissn=1098-1004&rft_id=info:doi/10.1002/humu.20074&rft_dat=%3Cproquest_cross%3E781202151%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=197274663&rft_id=info:pmid/15300848&rfr_iscdi=true |