Cigarette smoking and glutathione S-transferase M1 polymorphism associated with risk for uterine cervical cancer
Aim: To elucidate the role of tobacco smoking and polymorphisms of carcinogen metabolism genes in cervical carcinogenesis. Methods: We analyzed genotypes of nine genes, 11 polymorphisms encoding carcinogen metabolizing enzymes, information on smoking, and the presence of human papillomavirus in 12...
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| Veröffentlicht in: | The journal of obstetrics and gynaecology research 2008-12, Vol.34 (6), p.994-1001 |
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| creator | Nishino, Koji Sekine, Masayuki Kodama, Shoji Sudo, Norihito Aoki, Yoichi Seki, Nao Tanaka, Kenichi |
| description | Aim: To elucidate the role of tobacco smoking and polymorphisms of carcinogen metabolism genes in cervical carcinogenesis.
Methods: We analyzed genotypes of nine genes, 11 polymorphisms encoding carcinogen metabolizing enzymes, information on smoking, and the presence of human papillomavirus in 124 Japanese cervical cancer patients and 125 healthy controls.
Results: The incidence of human papillomavirus infection (95.5% vs 9.9%; P |
| doi_str_mv | 10.1111/j.1447-0756.2008.00798.x |
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Methods: We analyzed genotypes of nine genes, 11 polymorphisms encoding carcinogen metabolizing enzymes, information on smoking, and the presence of human papillomavirus in 124 Japanese cervical cancer patients and 125 healthy controls.
Results: The incidence of human papillomavirus infection (95.5% vs 9.9%; P < 0.001; odds ratio (OR), 231.98; 95% confidence interval [CI], 57.17–941.22), and smoking (41.1% vs 18.4%; P < 0.001; OR, 3.40; 95% CI, 1.88–6.17) were both significantly higher in patients than in controls. The genotype distributions of CYP1A1, CYP2E1, CYP2A6, NQO1, NAT2, mEH, MPO and GSTT1 genes were not statistically different; however, the ratio of the GSTM1 null genotype was significantly higher in patients than in controls (62.1% vs 47.2%; P = 0.019; OR, 1.83; 95% CI, 1.11–3.04). The incidence of GSTM1 null was significantly higher in the non‐smoking group (63.0% vs 47.1%; P = 0.038; OR, 1.92; 95% CI, 1.04–3.54), and not in the smoking group (60.8% vs 47.8%; P = 0.300; OR, 1.69; 95% CI, 0.63–4.56).
Conclusions: In the current study, risk factors for developing cervical cancer were tobacco smoking and GSTM1 null; however, no association was observed between these two factors. We could not prove that smoking–GSTM1 null interaction was responsible for the increase in cervical cancer among young Japanese, and further studies with more detailed smoking status, not only active but passive smoking, will be required.</description><identifier>ISSN: 1341-8076</identifier><identifier>EISSN: 1447-0756</identifier><identifier>DOI: 10.1111/j.1447-0756.2008.00798.x</identifier><identifier>PMID: 19012698</identifier><language>eng</language><publisher>Melbourne, Australia: Blackwell Publishing Asia</publisher><subject>Adult ; Cocarcinogenesis ; Female ; glutathione S-transferase M1 ; Glutathione Transferase - genetics ; human papilloma virus ; Human papillomavirus ; Humans ; Middle Aged ; Neoplasms, Squamous Cell - enzymology ; Neoplasms, Squamous Cell - etiology ; Neoplasms, Squamous Cell - genetics ; Neoplasms, Squamous Cell - virology ; Papillomaviridae - growth & development ; Papillomavirus Infections - virology ; polymorphism ; Polymorphism, Genetic ; smoking ; Smoking - adverse effects ; Smoking - genetics ; uterine cervical cancer ; Uterine Cervical Neoplasms - enzymology ; Uterine Cervical Neoplasms - etiology ; Uterine Cervical Neoplasms - genetics ; Uterine Cervical Neoplasms - virology</subject><ispartof>The journal of obstetrics and gynaecology research, 2008-12, Vol.34 (6), p.994-1001</ispartof><rights>2008 The Authors. Journal compilation © 2008 Japan Society of Obstetrics and Gynecology</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4888-523d482659c124e1db8a49d9abfa4755275ee335ca43441727b96e1716661a203</citedby><cites>FETCH-LOGICAL-c4888-523d482659c124e1db8a49d9abfa4755275ee335ca43441727b96e1716661a203</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1447-0756.2008.00798.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1447-0756.2008.00798.x$$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/19012698$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nishino, Koji</creatorcontrib><creatorcontrib>Sekine, Masayuki</creatorcontrib><creatorcontrib>Kodama, Shoji</creatorcontrib><creatorcontrib>Sudo, Norihito</creatorcontrib><creatorcontrib>Aoki, Yoichi</creatorcontrib><creatorcontrib>Seki, Nao</creatorcontrib><creatorcontrib>Tanaka, Kenichi</creatorcontrib><title>Cigarette smoking and glutathione S-transferase M1 polymorphism associated with risk for uterine cervical cancer</title><title>The journal of obstetrics and gynaecology research</title><addtitle>J Obstet Gynaecol Res</addtitle><description>Aim: To elucidate the role of tobacco smoking and polymorphisms of carcinogen metabolism genes in cervical carcinogenesis.
Methods: We analyzed genotypes of nine genes, 11 polymorphisms encoding carcinogen metabolizing enzymes, information on smoking, and the presence of human papillomavirus in 124 Japanese cervical cancer patients and 125 healthy controls.
Results: The incidence of human papillomavirus infection (95.5% vs 9.9%; P < 0.001; odds ratio (OR), 231.98; 95% confidence interval [CI], 57.17–941.22), and smoking (41.1% vs 18.4%; P < 0.001; OR, 3.40; 95% CI, 1.88–6.17) were both significantly higher in patients than in controls. The genotype distributions of CYP1A1, CYP2E1, CYP2A6, NQO1, NAT2, mEH, MPO and GSTT1 genes were not statistically different; however, the ratio of the GSTM1 null genotype was significantly higher in patients than in controls (62.1% vs 47.2%; P = 0.019; OR, 1.83; 95% CI, 1.11–3.04). The incidence of GSTM1 null was significantly higher in the non‐smoking group (63.0% vs 47.1%; P = 0.038; OR, 1.92; 95% CI, 1.04–3.54), and not in the smoking group (60.8% vs 47.8%; P = 0.300; OR, 1.69; 95% CI, 0.63–4.56).
Conclusions: In the current study, risk factors for developing cervical cancer were tobacco smoking and GSTM1 null; however, no association was observed between these two factors. We could not prove that smoking–GSTM1 null interaction was responsible for the increase in cervical cancer among young Japanese, and further studies with more detailed smoking status, not only active but passive smoking, will be required.</description><subject>Adult</subject><subject>Cocarcinogenesis</subject><subject>Female</subject><subject>glutathione S-transferase M1</subject><subject>Glutathione Transferase - genetics</subject><subject>human papilloma virus</subject><subject>Human papillomavirus</subject><subject>Humans</subject><subject>Middle Aged</subject><subject>Neoplasms, Squamous Cell - enzymology</subject><subject>Neoplasms, Squamous Cell - etiology</subject><subject>Neoplasms, Squamous Cell - genetics</subject><subject>Neoplasms, Squamous Cell - virology</subject><subject>Papillomaviridae - growth & development</subject><subject>Papillomavirus Infections - virology</subject><subject>polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>smoking</subject><subject>Smoking - adverse effects</subject><subject>Smoking - genetics</subject><subject>uterine cervical cancer</subject><subject>Uterine Cervical Neoplasms - enzymology</subject><subject>Uterine Cervical Neoplasms - etiology</subject><subject>Uterine Cervical Neoplasms - genetics</subject><subject>Uterine Cervical Neoplasms - virology</subject><issn>1341-8076</issn><issn>1447-0756</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE2P0zAQhi0EYj_gLyCfuCV4Ejt2JC5QsWVXhT3ALtwsN5m0bpM42M5u--9Jt9VyZS4z0rzPjPQQQoGlMNWHTQqcy4RJUaQZYyplTJYq3b0g58-Ll9Occ0gUk8UZuQhhwxjIEtRrcgYlg6wo1TkZZnZlPMaINHRua_sVNX1NV-0YTVxb1yP9kURv-tCgNwHpN6CDa_ed88Paho6aEFxlTcSaPtq4pt6GLW2cp2NEbye8Qv9gK9PSyvTT_Ia8akwb8O2pX5K7qy8_Z1-Txe38evZpkVRcKZWILK-5ygpRVpBxhHqpDC_r0iwbw6UQmRSIeS4qw3POQWZyWRYIEoqiAJOx_JK8P94dvPszYoi6s6HCtjU9ujHobDIgQckpqI7ByrsQPDZ68LYzfq-B6YNtvdEHqfogVR9s6yfbejeh704_xmWH9T_wpHcKfDwGHm2L-_8-rG9u5_IJT464DRF3z7jxW13IXAr96_tcC_is4PfNvV7kfwGV6Z2i</recordid><startdate>200812</startdate><enddate>200812</enddate><creator>Nishino, Koji</creator><creator>Sekine, Masayuki</creator><creator>Kodama, Shoji</creator><creator>Sudo, Norihito</creator><creator>Aoki, Yoichi</creator><creator>Seki, Nao</creator><creator>Tanaka, Kenichi</creator><general>Blackwell Publishing Asia</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>7U9</scope><scope>H94</scope></search><sort><creationdate>200812</creationdate><title>Cigarette smoking and glutathione S-transferase M1 polymorphism associated with risk for uterine cervical cancer</title><author>Nishino, Koji ; Sekine, Masayuki ; Kodama, Shoji ; Sudo, Norihito ; Aoki, Yoichi ; Seki, Nao ; Tanaka, Kenichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4888-523d482659c124e1db8a49d9abfa4755275ee335ca43441727b96e1716661a203</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adult</topic><topic>Cocarcinogenesis</topic><topic>Female</topic><topic>glutathione S-transferase M1</topic><topic>Glutathione Transferase - genetics</topic><topic>human papilloma virus</topic><topic>Human papillomavirus</topic><topic>Humans</topic><topic>Middle Aged</topic><topic>Neoplasms, Squamous Cell - enzymology</topic><topic>Neoplasms, Squamous Cell - etiology</topic><topic>Neoplasms, Squamous Cell - genetics</topic><topic>Neoplasms, Squamous Cell - virology</topic><topic>Papillomaviridae - growth & development</topic><topic>Papillomavirus Infections - virology</topic><topic>polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>smoking</topic><topic>Smoking - adverse effects</topic><topic>Smoking - genetics</topic><topic>uterine cervical cancer</topic><topic>Uterine Cervical Neoplasms - enzymology</topic><topic>Uterine Cervical Neoplasms - etiology</topic><topic>Uterine Cervical Neoplasms - genetics</topic><topic>Uterine Cervical Neoplasms - virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nishino, Koji</creatorcontrib><creatorcontrib>Sekine, Masayuki</creatorcontrib><creatorcontrib>Kodama, Shoji</creatorcontrib><creatorcontrib>Sudo, Norihito</creatorcontrib><creatorcontrib>Aoki, Yoichi</creatorcontrib><creatorcontrib>Seki, Nao</creatorcontrib><creatorcontrib>Tanaka, Kenichi</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>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>The journal of obstetrics and gynaecology research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nishino, Koji</au><au>Sekine, Masayuki</au><au>Kodama, Shoji</au><au>Sudo, Norihito</au><au>Aoki, Yoichi</au><au>Seki, Nao</au><au>Tanaka, Kenichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cigarette smoking and glutathione S-transferase M1 polymorphism associated with risk for uterine cervical cancer</atitle><jtitle>The journal of obstetrics and gynaecology research</jtitle><addtitle>J Obstet Gynaecol Res</addtitle><date>2008-12</date><risdate>2008</risdate><volume>34</volume><issue>6</issue><spage>994</spage><epage>1001</epage><pages>994-1001</pages><issn>1341-8076</issn><eissn>1447-0756</eissn><abstract>Aim: To elucidate the role of tobacco smoking and polymorphisms of carcinogen metabolism genes in cervical carcinogenesis.
Methods: We analyzed genotypes of nine genes, 11 polymorphisms encoding carcinogen metabolizing enzymes, information on smoking, and the presence of human papillomavirus in 124 Japanese cervical cancer patients and 125 healthy controls.
Results: The incidence of human papillomavirus infection (95.5% vs 9.9%; P < 0.001; odds ratio (OR), 231.98; 95% confidence interval [CI], 57.17–941.22), and smoking (41.1% vs 18.4%; P < 0.001; OR, 3.40; 95% CI, 1.88–6.17) were both significantly higher in patients than in controls. The genotype distributions of CYP1A1, CYP2E1, CYP2A6, NQO1, NAT2, mEH, MPO and GSTT1 genes were not statistically different; however, the ratio of the GSTM1 null genotype was significantly higher in patients than in controls (62.1% vs 47.2%; P = 0.019; OR, 1.83; 95% CI, 1.11–3.04). The incidence of GSTM1 null was significantly higher in the non‐smoking group (63.0% vs 47.1%; P = 0.038; OR, 1.92; 95% CI, 1.04–3.54), and not in the smoking group (60.8% vs 47.8%; P = 0.300; OR, 1.69; 95% CI, 0.63–4.56).
Conclusions: In the current study, risk factors for developing cervical cancer were tobacco smoking and GSTM1 null; however, no association was observed between these two factors. We could not prove that smoking–GSTM1 null interaction was responsible for the increase in cervical cancer among young Japanese, and further studies with more detailed smoking status, not only active but passive smoking, will be required.</abstract><cop>Melbourne, Australia</cop><pub>Blackwell Publishing Asia</pub><pmid>19012698</pmid><doi>10.1111/j.1447-0756.2008.00798.x</doi><tpages>8</tpages></addata></record> |
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| subjects | Adult Cocarcinogenesis Female glutathione S-transferase M1 Glutathione Transferase - genetics human papilloma virus Human papillomavirus Humans Middle Aged Neoplasms, Squamous Cell - enzymology Neoplasms, Squamous Cell - etiology Neoplasms, Squamous Cell - genetics Neoplasms, Squamous Cell - virology Papillomaviridae - growth & development Papillomavirus Infections - virology polymorphism Polymorphism, Genetic smoking Smoking - adverse effects Smoking - genetics uterine cervical cancer Uterine Cervical Neoplasms - enzymology Uterine Cervical Neoplasms - etiology Uterine Cervical Neoplasms - genetics Uterine Cervical Neoplasms - virology |
| title | Cigarette smoking and glutathione S-transferase M1 polymorphism associated with risk for uterine cervical cancer |
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