Polymorphisms of GSTP1 and GSTT1, but not of CYP2A6, CYP2E1 or GSTM1, modify the risk for esophageal cancer in a western population
Esophageal cancer is among the most common and fatal tumors in the world. Eighty percent of esophageal tumors are esophageal squamous cell carcinoma (ESCC). Brazil is one of the high incidence areas in the West, where tobacco and alcohol consumption have been associated with ESCC. However, polymorph...
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| Veröffentlicht in: | Carcinogenesis (New York) 2007-12, Vol.28 (12), p.2537-2542 |
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| creator | Rossini, A. Rapozo, D.C.M. Soares Lima, S.C. Guimarães, D.P. Ferreira, M.A. Teixeira, R. Kruel, C.D.P. Barros, S.G.S. Andreollo, N.A. Acatauassú, R. Matos, H.J. Albano, R.M. Pinto, L.F.Ribeiro |
| description | Esophageal cancer is among the most common and fatal tumors in the world. Eighty percent of esophageal tumors are esophageal squamous cell carcinoma (ESCC). Brazil is one of the high incidence areas in the West, where tobacco and alcohol consumption have been associated with ESCC. However, polymorphisms in xenobiotic metabolizing genes may also contribute to the risk. Therefore, in this study, we analyzed the risk of ESCC associated with tobacco and alcohol consumption and with polymorphisms of CYP2A6 (CYP2A6*2), CYP2E1 (CYP2E1*5B, CYP2E1*6), GSTP1 (Ile105Val), GSTM1 and GSTT1 null genotypes in 126 cases and 252 age- and gender-matched controls. Data on the amount, length and type of tobacco and alcohol consumed were collected, and DNA was extracted from blood lymphocytes from all individuals. Polymorphisms were analyzed by polymerase chain reaction (PCR)–multiplex (GSTM1 and T1), PCR–Restriction Fragment Length Polymorphism (CYP2E1*5B and *6 and GSTP1 Ile105Val) or allele-specific PCR amplification (CYP2A6*2). Risks were evaluated by multivariate conditional regression analysis. As expected, tobacco [odds ratio (OR) = 6.71, 95% confidence interval (95% CI) 3.08–14.63] and alcohol (OR = 16.98, CI 7.8–36.98) consumption, independently or together (OR = 26.91, CI 13.39–54.05) were risk factors. GSTP1 Ile105Val polymorphism was an independent risk factor (OR = 2.12, CI 1.37–3.29), whereas GSTT1 wild-type was an independent protective factor for ESCC (OR = 0.37, CI 0.16–0.79). There was ∼80% statistical power to detect both results. There was no risk associated with CYP2A6, CYP2E1 and GSTM1 polymorphisms. In conclusion, this study suggests an opposite role of GSTP1 and GSTT1 polymorphisms for the risk for ESCC. |
| doi_str_mv | 10.1093/carcin/bgm222 |
| format | Article |
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Eighty percent of esophageal tumors are esophageal squamous cell carcinoma (ESCC). Brazil is one of the high incidence areas in the West, where tobacco and alcohol consumption have been associated with ESCC. However, polymorphisms in xenobiotic metabolizing genes may also contribute to the risk. Therefore, in this study, we analyzed the risk of ESCC associated with tobacco and alcohol consumption and with polymorphisms of CYP2A6 (CYP2A6*2), CYP2E1 (CYP2E1*5B, CYP2E1*6), GSTP1 (Ile105Val), GSTM1 and GSTT1 null genotypes in 126 cases and 252 age- and gender-matched controls. Data on the amount, length and type of tobacco and alcohol consumed were collected, and DNA was extracted from blood lymphocytes from all individuals. Polymorphisms were analyzed by polymerase chain reaction (PCR)–multiplex (GSTM1 and T1), PCR–Restriction Fragment Length Polymorphism (CYP2E1*5B and *6 and GSTP1 Ile105Val) or allele-specific PCR amplification (CYP2A6*2). Risks were evaluated by multivariate conditional regression analysis. As expected, tobacco [odds ratio (OR) = 6.71, 95% confidence interval (95% CI) 3.08–14.63] and alcohol (OR = 16.98, CI 7.8–36.98) consumption, independently or together (OR = 26.91, CI 13.39–54.05) were risk factors. GSTP1 Ile105Val polymorphism was an independent risk factor (OR = 2.12, CI 1.37–3.29), whereas GSTT1 wild-type was an independent protective factor for ESCC (OR = 0.37, CI 0.16–0.79). There was ∼80% statistical power to detect both results. There was no risk associated with CYP2A6, CYP2E1 and GSTM1 polymorphisms. In conclusion, this study suggests an opposite role of GSTP1 and GSTT1 polymorphisms for the risk for ESCC.</description><identifier>ISSN: 0143-3334</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/bgm222</identifier><identifier>PMID: 17916905</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Alcohol Drinking ; Aryl Hydrocarbon Hydroxylases - genetics ; Biological and medical sciences ; Brazil ; Carcinogenesis, carcinogens and anticarcinogens ; Case-Control Studies ; Cytochrome P-450 CYP2A6 ; Cytochrome P-450 CYP2E1 - genetics ; Esophageal Neoplasms - genetics ; Female ; Glutathione S-Transferase pi - genetics ; Glutathione Transferase - genetics ; Humans ; Male ; Medical sciences ; Middle Aged ; Mixed Function Oxygenases - genetics ; Polymorphism, Genetic ; Risk Factors ; Smoking ; Tumors</subject><ispartof>Carcinogenesis (New York), 2007-12, Vol.28 (12), p.2537-2542</ispartof><rights>The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org 2007</rights><rights>2008 INIST-CNRS</rights><rights>The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c450t-1536592dcbe352f32ff213f29546c2884bc0bc07fda4ff73fbd3d41b519ebe753</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1578,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19914554$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17916905$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rossini, A.</creatorcontrib><creatorcontrib>Rapozo, D.C.M.</creatorcontrib><creatorcontrib>Soares Lima, S.C.</creatorcontrib><creatorcontrib>Guimarães, D.P.</creatorcontrib><creatorcontrib>Ferreira, M.A.</creatorcontrib><creatorcontrib>Teixeira, R.</creatorcontrib><creatorcontrib>Kruel, C.D.P.</creatorcontrib><creatorcontrib>Barros, S.G.S.</creatorcontrib><creatorcontrib>Andreollo, N.A.</creatorcontrib><creatorcontrib>Acatauassú, R.</creatorcontrib><creatorcontrib>Matos, H.J.</creatorcontrib><creatorcontrib>Albano, R.M.</creatorcontrib><creatorcontrib>Pinto, L.F.Ribeiro</creatorcontrib><title>Polymorphisms of GSTP1 and GSTT1, but not of CYP2A6, CYP2E1 or GSTM1, modify the risk for esophageal cancer in a western population</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>Esophageal cancer is among the most common and fatal tumors in the world. Eighty percent of esophageal tumors are esophageal squamous cell carcinoma (ESCC). Brazil is one of the high incidence areas in the West, where tobacco and alcohol consumption have been associated with ESCC. However, polymorphisms in xenobiotic metabolizing genes may also contribute to the risk. Therefore, in this study, we analyzed the risk of ESCC associated with tobacco and alcohol consumption and with polymorphisms of CYP2A6 (CYP2A6*2), CYP2E1 (CYP2E1*5B, CYP2E1*6), GSTP1 (Ile105Val), GSTM1 and GSTT1 null genotypes in 126 cases and 252 age- and gender-matched controls. Data on the amount, length and type of tobacco and alcohol consumed were collected, and DNA was extracted from blood lymphocytes from all individuals. Polymorphisms were analyzed by polymerase chain reaction (PCR)–multiplex (GSTM1 and T1), PCR–Restriction Fragment Length Polymorphism (CYP2E1*5B and *6 and GSTP1 Ile105Val) or allele-specific PCR amplification (CYP2A6*2). Risks were evaluated by multivariate conditional regression analysis. As expected, tobacco [odds ratio (OR) = 6.71, 95% confidence interval (95% CI) 3.08–14.63] and alcohol (OR = 16.98, CI 7.8–36.98) consumption, independently or together (OR = 26.91, CI 13.39–54.05) were risk factors. GSTP1 Ile105Val polymorphism was an independent risk factor (OR = 2.12, CI 1.37–3.29), whereas GSTT1 wild-type was an independent protective factor for ESCC (OR = 0.37, CI 0.16–0.79). There was ∼80% statistical power to detect both results. There was no risk associated with CYP2A6, CYP2E1 and GSTM1 polymorphisms. In conclusion, this study suggests an opposite role of GSTP1 and GSTT1 polymorphisms for the risk for ESCC.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alcohol Drinking</subject><subject>Aryl Hydrocarbon Hydroxylases - genetics</subject><subject>Biological and medical sciences</subject><subject>Brazil</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>Case-Control Studies</subject><subject>Cytochrome P-450 CYP2A6</subject><subject>Cytochrome P-450 CYP2E1 - genetics</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Female</subject><subject>Glutathione S-Transferase pi - genetics</subject><subject>Glutathione Transferase - genetics</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mixed Function Oxygenases - genetics</subject><subject>Polymorphism, Genetic</subject><subject>Risk Factors</subject><subject>Smoking</subject><subject>Tumors</subject><issn>0143-3334</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0c-L1DAUB_AgijuuHr1KEBQPWzc_2-a4zK47woqDO4J6CWma7GS3bWrSonP2Hze1xQUvQuAF3ofk8b4APMfoLUaCnmoVtOtOq5uWEPIArDDLUUZwiR6CFcKMZpRSdgSexHiLEM4pF4_BES4EzgXiK_Br65tD60O_d7GN0Ft4eb3bYqi6errt8AmsxgF2fph6669bcpaf_KkXGPowmQ_JtL529gCHvYHBxTtoU8tE3-_VjVEN1KrTJkDXQQV_mDiY0MHe92OjBue7p-CRVU00z5Z6DD6_u9itN9nVx8v367OrTDOOhgxzmnNBal0ZyomlxFqCqSWCs1yTsmSVRukUtlbM2oLaqqY1wxXHwlSm4PQYvJ7f7YP_PqYxZOuiNk2jOuPHKAliaSnlBF_-A2_9GLo0myRY0IKxokwom5EOPsZgrOyDa1U4SIzkFI2co5FzNMm_WB4dq9bU93rJIoFXC1BRq8aGtDQX750QmHHOknszOz_2__1zmdGlnf_8i1W4k3lBCy43X77J4vr80_p8U8od_Q1dULL1</recordid><startdate>20071201</startdate><enddate>20071201</enddate><creator>Rossini, A.</creator><creator>Rapozo, D.C.M.</creator><creator>Soares Lima, S.C.</creator><creator>Guimarães, D.P.</creator><creator>Ferreira, M.A.</creator><creator>Teixeira, R.</creator><creator>Kruel, C.D.P.</creator><creator>Barros, S.G.S.</creator><creator>Andreollo, N.A.</creator><creator>Acatauassú, R.</creator><creator>Matos, H.J.</creator><creator>Albano, R.M.</creator><creator>Pinto, L.F.Ribeiro</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>20071201</creationdate><title>Polymorphisms of GSTP1 and GSTT1, but not of CYP2A6, CYP2E1 or GSTM1, modify the risk for esophageal cancer in a western population</title><author>Rossini, A. ; Rapozo, D.C.M. ; Soares Lima, S.C. ; Guimarães, D.P. ; Ferreira, M.A. ; Teixeira, R. ; Kruel, C.D.P. ; Barros, S.G.S. ; Andreollo, N.A. ; Acatauassú, R. ; Matos, H.J. ; Albano, R.M. ; Pinto, L.F.Ribeiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c450t-1536592dcbe352f32ff213f29546c2884bc0bc07fda4ff73fbd3d41b519ebe753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alcohol Drinking</topic><topic>Aryl Hydrocarbon Hydroxylases - genetics</topic><topic>Biological and medical sciences</topic><topic>Brazil</topic><topic>Carcinogenesis, carcinogens and anticarcinogens</topic><topic>Case-Control Studies</topic><topic>Cytochrome P-450 CYP2A6</topic><topic>Cytochrome P-450 CYP2E1 - genetics</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Female</topic><topic>Glutathione S-Transferase pi - genetics</topic><topic>Glutathione Transferase - genetics</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mixed Function Oxygenases - genetics</topic><topic>Polymorphism, Genetic</topic><topic>Risk Factors</topic><topic>Smoking</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rossini, A.</creatorcontrib><creatorcontrib>Rapozo, D.C.M.</creatorcontrib><creatorcontrib>Soares Lima, S.C.</creatorcontrib><creatorcontrib>Guimarães, D.P.</creatorcontrib><creatorcontrib>Ferreira, M.A.</creatorcontrib><creatorcontrib>Teixeira, R.</creatorcontrib><creatorcontrib>Kruel, C.D.P.</creatorcontrib><creatorcontrib>Barros, S.G.S.</creatorcontrib><creatorcontrib>Andreollo, N.A.</creatorcontrib><creatorcontrib>Acatauassú, R.</creatorcontrib><creatorcontrib>Matos, H.J.</creatorcontrib><creatorcontrib>Albano, R.M.</creatorcontrib><creatorcontrib>Pinto, L.F.Ribeiro</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>Rossini, A.</au><au>Rapozo, D.C.M.</au><au>Soares Lima, S.C.</au><au>Guimarães, D.P.</au><au>Ferreira, M.A.</au><au>Teixeira, R.</au><au>Kruel, C.D.P.</au><au>Barros, S.G.S.</au><au>Andreollo, N.A.</au><au>Acatauassú, R.</au><au>Matos, H.J.</au><au>Albano, R.M.</au><au>Pinto, L.F.Ribeiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Polymorphisms of GSTP1 and GSTT1, but not of CYP2A6, CYP2E1 or GSTM1, modify the risk for esophageal cancer in a western population</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>2007-12-01</date><risdate>2007</risdate><volume>28</volume><issue>12</issue><spage>2537</spage><epage>2542</epage><pages>2537-2542</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract>Esophageal cancer is among the most common and fatal tumors in the world. Eighty percent of esophageal tumors are esophageal squamous cell carcinoma (ESCC). Brazil is one of the high incidence areas in the West, where tobacco and alcohol consumption have been associated with ESCC. However, polymorphisms in xenobiotic metabolizing genes may also contribute to the risk. Therefore, in this study, we analyzed the risk of ESCC associated with tobacco and alcohol consumption and with polymorphisms of CYP2A6 (CYP2A6*2), CYP2E1 (CYP2E1*5B, CYP2E1*6), GSTP1 (Ile105Val), GSTM1 and GSTT1 null genotypes in 126 cases and 252 age- and gender-matched controls. Data on the amount, length and type of tobacco and alcohol consumed were collected, and DNA was extracted from blood lymphocytes from all individuals. Polymorphisms were analyzed by polymerase chain reaction (PCR)–multiplex (GSTM1 and T1), PCR–Restriction Fragment Length Polymorphism (CYP2E1*5B and *6 and GSTP1 Ile105Val) or allele-specific PCR amplification (CYP2A6*2). Risks were evaluated by multivariate conditional regression analysis. As expected, tobacco [odds ratio (OR) = 6.71, 95% confidence interval (95% CI) 3.08–14.63] and alcohol (OR = 16.98, CI 7.8–36.98) consumption, independently or together (OR = 26.91, CI 13.39–54.05) were risk factors. GSTP1 Ile105Val polymorphism was an independent risk factor (OR = 2.12, CI 1.37–3.29), whereas GSTT1 wild-type was an independent protective factor for ESCC (OR = 0.37, CI 0.16–0.79). There was ∼80% statistical power to detect both results. There was no risk associated with CYP2A6, CYP2E1 and GSTM1 polymorphisms. In conclusion, this study suggests an opposite role of GSTP1 and GSTT1 polymorphisms for the risk for ESCC.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>17916905</pmid><doi>10.1093/carcin/bgm222</doi><tpages>6</tpages></addata></record> |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adult Aged Aged, 80 and over Alcohol Drinking Aryl Hydrocarbon Hydroxylases - genetics Biological and medical sciences Brazil Carcinogenesis, carcinogens and anticarcinogens Case-Control Studies Cytochrome P-450 CYP2A6 Cytochrome P-450 CYP2E1 - genetics Esophageal Neoplasms - genetics Female Glutathione S-Transferase pi - genetics Glutathione Transferase - genetics Humans Male Medical sciences Middle Aged Mixed Function Oxygenases - genetics Polymorphism, Genetic Risk Factors Smoking Tumors |
| title | Polymorphisms of GSTP1 and GSTT1, but not of CYP2A6, CYP2E1 or GSTM1, modify the risk for esophageal cancer in a western population |
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