Effect of heme oxygenase‐1 gene promoter polymorphism on cancer risk by histological subtype: A prospective study in arseniasis‐endemic areas in Taiwan
Heme oxygenase (HO)−1 is upregulated by many stressful stimuli, including arsenic. A GT‐repeat ((GT)n) polymorphism in the HO‐1 gene promoter inversely modulates the levels of HO‐1 induction. Previous HO‐1 (GT)n polymorphism studies in relation to cancer risk have shown disparate results. We prospec...
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| Veröffentlicht in: | International journal of cancer 2016-04, Vol.138 (8), p.1875-1886 |
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| creator | Wu, Meei‐Maan Lee, Chih‐Hung Hsu, Ling‐I Cheng, Wen‐Fang Lee, Te‐Chang Wang, Yuang‐Hung Chiou, Hung‐Yi Chen, Chien‐Jen |
| description | Heme oxygenase (HO)−1 is upregulated by many stressful stimuli, including arsenic. A GT‐repeat ((GT)n) polymorphism in the HO‐1 gene promoter inversely modulates the levels of HO‐1 induction. Previous HO‐1 (GT)n polymorphism studies in relation to cancer risk have shown disparate results. We prospectively investigated the associations between HO‐1 (GT)n polymorphism and cancer risk related to arsenic from drinking water. Totally, 1,013 participants from community‐based cohorts of arseniasis‐endemic areas in Taiwan were followed for 13 years. Allelic polymorphisms were classified into long (L, ≥27 (GT)n) and short (S, |
| doi_str_mv | 10.1002/ijc.29926 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_1919968807</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1764139059</sourcerecordid><originalsourceid>FETCH-LOGICAL-p3476-800e40d4542a95f1990b4e4402b3827b7be1e7039935aa874882053cf595c663</originalsourceid><addsrcrecordid>eNqFkc1u1DAUhS0EokNhwQsgS2y6SXvt-CdmV40KLarUzewjx3PTekjsECeU7PoI7Hk7nqSetrBg05Wvzvl8f3QIec_gmAHwE79zx9wYrl6QFQOjC-BMviSr7EGhWakOyJuUdgCMSRCvyQFXUikN1Yr8PmtbdBONLb3BHmn8uVxjsAn_3P1iNJdIhzH2ccKRDrFb-jgONz71NAbqbHBZHn36RpuFZnmKXbz2znY0zc20DPiJnu7_pyHP8D-QpmneLtQHaseEwdvkUx6EYYu9d1lEm_buxvpbG96SV63tEr57eg_J5vPZZn1eXF59uVifXhZDKbQqKgAUsBVScGtky4yBRqAQwJuy4rrRDTLUUBpTSmsrLaqKgyxdK410SpWH5OixbV70-4xpqnufHHadDRjnVDOTW6qqAv08qpVgpQFpMvrxP3QX5zHkO_YUz7toAZn68ETNTY_behh9b8el_htQBk4egVvf4fLPZ1Dvk69z8vVD8vXF1_VDUd4DRZKiRg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1762935740</pqid></control><display><type>article</type><title>Effect of heme oxygenase‐1 gene promoter polymorphism on cancer risk by histological subtype: A prospective study in arseniasis‐endemic areas in Taiwan</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Wu, Meei‐Maan ; Lee, Chih‐Hung ; Hsu, Ling‐I ; Cheng, Wen‐Fang ; Lee, Te‐Chang ; Wang, Yuang‐Hung ; Chiou, Hung‐Yi ; Chen, Chien‐Jen</creator><creatorcontrib>Wu, Meei‐Maan ; Lee, Chih‐Hung ; Hsu, Ling‐I ; Cheng, Wen‐Fang ; Lee, Te‐Chang ; Wang, Yuang‐Hung ; Chiou, Hung‐Yi ; Chen, Chien‐Jen</creatorcontrib><description>Heme oxygenase (HO)−1 is upregulated by many stressful stimuli, including arsenic. A GT‐repeat ((GT)n) polymorphism in the HO‐1 gene promoter inversely modulates the levels of HO‐1 induction. Previous HO‐1 (GT)n polymorphism studies in relation to cancer risk have shown disparate results. We prospectively investigated the associations between HO‐1 (GT)n polymorphism and cancer risk related to arsenic from drinking water. Totally, 1,013 participants from community‐based cohorts of arseniasis‐endemic areas in Taiwan were followed for 13 years. Allelic polymorphisms were classified into long (L, ≥27 (GT)n) and short (S, <27 (GT)n). Newly developed cases were identified through linkage with National Cancer Registry of Taiwan. Multivariate Cox proportional hazard methods were used to evaluate effects of the HO‐1 polymorphism alone or combined with arsenic exposure. Results showed that participants with the S/S genotype had an increased risk of Bowen's disease (HR = 10.49; 95% CI: 2.77–39.7), invasive skin cancer (HR = 2.99; 95% CI: 1.13–7.87), and lung squamous cell carcinoma (HR = 3.39; 95% CI: 1.15–9.95) versus those with L/S or L/L genotype. The S/S genotype combined with high arsenic exposure (>300 μg/L) had a greater risk of skin cancer compared to the genotype alone. Consistent with previous findings, participants with the S‐allele had a reduced risk of lung adenocarcinoma (HR = 0.21; 95% CI: 0.03–0.68) versus those with L/L genotype. There were no significant differences in risk of urothelial carcinoma among the three genotypes. Associations of HO‐1 (GT)n polymorphism with cancer risk differs by histological subtype and the polymorphism should be considered a modifier in the risk assessment of arsenic exposure.
What's new?
Heme oxygenase (HO)−1 defends cells against oxidative stress, but its protective effects are modulated by polymorphisms that shorten or lengthen the number of GT dinucleotide repeats in the gene promoter. Here, among cohorts in areas of Taiwan affected by endemic arsenic poisoning, individuals who were homozygous for short (GT)n polymorphisms (S/S, <27 dinucleotide repeats) were found to be at increased risk of skin cancer and lung squamous cell carcinoma. Arsenic exposure further increased skin cancer risk among S/S individuals. All S‐allele carriers, however, had a reduced risk of lung adenocarcinoma, a malignancy unrelated to arsenic exposure.</description><identifier>ISSN: 0020-7136</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/ijc.29926</identifier><identifier>PMID: 26566708</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Arsenic ; arsenic exposure ; Arsenic Poisoning - complications ; Arsenic Poisoning - epidemiology ; Arsenic Poisoning - genetics ; Bowen's disease ; Cancer ; cancer risk ; Drinking Water - adverse effects ; Endemic Diseases ; Female ; Fluorescent Antibody Technique ; genetic polymorphism ; Genetic Predisposition to Disease - genetics ; Genotype ; Genotype & phenotype ; Heme Oxygenase-1 - genetics ; heme oxygenase‐1 ; Histology ; Humans ; Incidence ; Lung cancer ; Male ; Medical research ; Middle Aged ; Neoplasms - chemically induced ; Neoplasms - enzymology ; Neoplasms - genetics ; Polymorphism ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic - genetics ; Proportional Hazards Models ; Prospective Studies ; Reverse Transcriptase Polymerase Chain Reaction ; Risk factors ; Taiwan - epidemiology</subject><ispartof>International journal of cancer, 2016-04, Vol.138 (8), p.1875-1886</ispartof><rights>2015 UICC</rights><rights>2015 UICC.</rights><rights>2016 UICC</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fijc.29926$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fijc.29926$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26566708$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Meei‐Maan</creatorcontrib><creatorcontrib>Lee, Chih‐Hung</creatorcontrib><creatorcontrib>Hsu, Ling‐I</creatorcontrib><creatorcontrib>Cheng, Wen‐Fang</creatorcontrib><creatorcontrib>Lee, Te‐Chang</creatorcontrib><creatorcontrib>Wang, Yuang‐Hung</creatorcontrib><creatorcontrib>Chiou, Hung‐Yi</creatorcontrib><creatorcontrib>Chen, Chien‐Jen</creatorcontrib><title>Effect of heme oxygenase‐1 gene promoter polymorphism on cancer risk by histological subtype: A prospective study in arseniasis‐endemic areas in Taiwan</title><title>International journal of cancer</title><addtitle>Int J Cancer</addtitle><description>Heme oxygenase (HO)−1 is upregulated by many stressful stimuli, including arsenic. A GT‐repeat ((GT)n) polymorphism in the HO‐1 gene promoter inversely modulates the levels of HO‐1 induction. Previous HO‐1 (GT)n polymorphism studies in relation to cancer risk have shown disparate results. We prospectively investigated the associations between HO‐1 (GT)n polymorphism and cancer risk related to arsenic from drinking water. Totally, 1,013 participants from community‐based cohorts of arseniasis‐endemic areas in Taiwan were followed for 13 years. Allelic polymorphisms were classified into long (L, ≥27 (GT)n) and short (S, <27 (GT)n). Newly developed cases were identified through linkage with National Cancer Registry of Taiwan. Multivariate Cox proportional hazard methods were used to evaluate effects of the HO‐1 polymorphism alone or combined with arsenic exposure. Results showed that participants with the S/S genotype had an increased risk of Bowen's disease (HR = 10.49; 95% CI: 2.77–39.7), invasive skin cancer (HR = 2.99; 95% CI: 1.13–7.87), and lung squamous cell carcinoma (HR = 3.39; 95% CI: 1.15–9.95) versus those with L/S or L/L genotype. The S/S genotype combined with high arsenic exposure (>300 μg/L) had a greater risk of skin cancer compared to the genotype alone. Consistent with previous findings, participants with the S‐allele had a reduced risk of lung adenocarcinoma (HR = 0.21; 95% CI: 0.03–0.68) versus those with L/L genotype. There were no significant differences in risk of urothelial carcinoma among the three genotypes. Associations of HO‐1 (GT)n polymorphism with cancer risk differs by histological subtype and the polymorphism should be considered a modifier in the risk assessment of arsenic exposure.
What's new?
Heme oxygenase (HO)−1 defends cells against oxidative stress, but its protective effects are modulated by polymorphisms that shorten or lengthen the number of GT dinucleotide repeats in the gene promoter. Here, among cohorts in areas of Taiwan affected by endemic arsenic poisoning, individuals who were homozygous for short (GT)n polymorphisms (S/S, <27 dinucleotide repeats) were found to be at increased risk of skin cancer and lung squamous cell carcinoma. Arsenic exposure further increased skin cancer risk among S/S individuals. All S‐allele carriers, however, had a reduced risk of lung adenocarcinoma, a malignancy unrelated to arsenic exposure.</description><subject>Arsenic</subject><subject>arsenic exposure</subject><subject>Arsenic Poisoning - complications</subject><subject>Arsenic Poisoning - epidemiology</subject><subject>Arsenic Poisoning - genetics</subject><subject>Bowen's disease</subject><subject>Cancer</subject><subject>cancer risk</subject><subject>Drinking Water - adverse effects</subject><subject>Endemic Diseases</subject><subject>Female</subject><subject>Fluorescent Antibody Technique</subject><subject>genetic polymorphism</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>Heme Oxygenase-1 - genetics</subject><subject>heme oxygenase‐1</subject><subject>Histology</subject><subject>Humans</subject><subject>Incidence</subject><subject>Lung cancer</subject><subject>Male</subject><subject>Medical research</subject><subject>Middle Aged</subject><subject>Neoplasms - chemically induced</subject><subject>Neoplasms - enzymology</subject><subject>Neoplasms - genetics</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Proportional Hazards Models</subject><subject>Prospective Studies</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Risk factors</subject><subject>Taiwan - epidemiology</subject><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1DAUhS0EokNhwQsgS2y6SXvt-CdmV40KLarUzewjx3PTekjsECeU7PoI7Hk7nqSetrBg05Wvzvl8f3QIec_gmAHwE79zx9wYrl6QFQOjC-BMviSr7EGhWakOyJuUdgCMSRCvyQFXUikN1Yr8PmtbdBONLb3BHmn8uVxjsAn_3P1iNJdIhzH2ccKRDrFb-jgONz71NAbqbHBZHn36RpuFZnmKXbz2znY0zc20DPiJnu7_pyHP8D-QpmneLtQHaseEwdvkUx6EYYu9d1lEm_buxvpbG96SV63tEr57eg_J5vPZZn1eXF59uVifXhZDKbQqKgAUsBVScGtky4yBRqAQwJuy4rrRDTLUUBpTSmsrLaqKgyxdK410SpWH5OixbV70-4xpqnufHHadDRjnVDOTW6qqAv08qpVgpQFpMvrxP3QX5zHkO_YUz7toAZn68ETNTY_behh9b8el_htQBk4egVvf4fLPZ1Dvk69z8vVD8vXF1_VDUd4DRZKiRg</recordid><startdate>20160415</startdate><enddate>20160415</enddate><creator>Wu, Meei‐Maan</creator><creator>Lee, Chih‐Hung</creator><creator>Hsu, Ling‐I</creator><creator>Cheng, Wen‐Fang</creator><creator>Lee, Te‐Chang</creator><creator>Wang, Yuang‐Hung</creator><creator>Chiou, Hung‐Yi</creator><creator>Chen, Chien‐Jen</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20160415</creationdate><title>Effect of heme oxygenase‐1 gene promoter polymorphism on cancer risk by histological subtype: A prospective study in arseniasis‐endemic areas in Taiwan</title><author>Wu, Meei‐Maan ; Lee, Chih‐Hung ; Hsu, Ling‐I ; Cheng, Wen‐Fang ; Lee, Te‐Chang ; Wang, Yuang‐Hung ; Chiou, Hung‐Yi ; Chen, Chien‐Jen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p3476-800e40d4542a95f1990b4e4402b3827b7be1e7039935aa874882053cf595c663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Arsenic</topic><topic>arsenic exposure</topic><topic>Arsenic Poisoning - complications</topic><topic>Arsenic Poisoning - epidemiology</topic><topic>Arsenic Poisoning - genetics</topic><topic>Bowen's disease</topic><topic>Cancer</topic><topic>cancer risk</topic><topic>Drinking Water - adverse effects</topic><topic>Endemic Diseases</topic><topic>Female</topic><topic>Fluorescent Antibody Technique</topic><topic>genetic polymorphism</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Genotype</topic><topic>Genotype & phenotype</topic><topic>Heme Oxygenase-1 - genetics</topic><topic>heme oxygenase‐1</topic><topic>Histology</topic><topic>Humans</topic><topic>Incidence</topic><topic>Lung cancer</topic><topic>Male</topic><topic>Medical research</topic><topic>Middle Aged</topic><topic>Neoplasms - chemically induced</topic><topic>Neoplasms - enzymology</topic><topic>Neoplasms - genetics</topic><topic>Polymorphism</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Proportional Hazards Models</topic><topic>Prospective Studies</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Risk factors</topic><topic>Taiwan - epidemiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Meei‐Maan</creatorcontrib><creatorcontrib>Lee, Chih‐Hung</creatorcontrib><creatorcontrib>Hsu, Ling‐I</creatorcontrib><creatorcontrib>Cheng, Wen‐Fang</creatorcontrib><creatorcontrib>Lee, Te‐Chang</creatorcontrib><creatorcontrib>Wang, Yuang‐Hung</creatorcontrib><creatorcontrib>Chiou, Hung‐Yi</creatorcontrib><creatorcontrib>Chen, Chien‐Jen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>International journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Meei‐Maan</au><au>Lee, Chih‐Hung</au><au>Hsu, Ling‐I</au><au>Cheng, Wen‐Fang</au><au>Lee, Te‐Chang</au><au>Wang, Yuang‐Hung</au><au>Chiou, Hung‐Yi</au><au>Chen, Chien‐Jen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of heme oxygenase‐1 gene promoter polymorphism on cancer risk by histological subtype: A prospective study in arseniasis‐endemic areas in Taiwan</atitle><jtitle>International journal of cancer</jtitle><addtitle>Int J Cancer</addtitle><date>2016-04-15</date><risdate>2016</risdate><volume>138</volume><issue>8</issue><spage>1875</spage><epage>1886</epage><pages>1875-1886</pages><issn>0020-7136</issn><eissn>1097-0215</eissn><abstract>Heme oxygenase (HO)−1 is upregulated by many stressful stimuli, including arsenic. A GT‐repeat ((GT)n) polymorphism in the HO‐1 gene promoter inversely modulates the levels of HO‐1 induction. Previous HO‐1 (GT)n polymorphism studies in relation to cancer risk have shown disparate results. We prospectively investigated the associations between HO‐1 (GT)n polymorphism and cancer risk related to arsenic from drinking water. Totally, 1,013 participants from community‐based cohorts of arseniasis‐endemic areas in Taiwan were followed for 13 years. Allelic polymorphisms were classified into long (L, ≥27 (GT)n) and short (S, <27 (GT)n). Newly developed cases were identified through linkage with National Cancer Registry of Taiwan. Multivariate Cox proportional hazard methods were used to evaluate effects of the HO‐1 polymorphism alone or combined with arsenic exposure. Results showed that participants with the S/S genotype had an increased risk of Bowen's disease (HR = 10.49; 95% CI: 2.77–39.7), invasive skin cancer (HR = 2.99; 95% CI: 1.13–7.87), and lung squamous cell carcinoma (HR = 3.39; 95% CI: 1.15–9.95) versus those with L/S or L/L genotype. The S/S genotype combined with high arsenic exposure (>300 μg/L) had a greater risk of skin cancer compared to the genotype alone. Consistent with previous findings, participants with the S‐allele had a reduced risk of lung adenocarcinoma (HR = 0.21; 95% CI: 0.03–0.68) versus those with L/L genotype. There were no significant differences in risk of urothelial carcinoma among the three genotypes. Associations of HO‐1 (GT)n polymorphism with cancer risk differs by histological subtype and the polymorphism should be considered a modifier in the risk assessment of arsenic exposure.
What's new?
Heme oxygenase (HO)−1 defends cells against oxidative stress, but its protective effects are modulated by polymorphisms that shorten or lengthen the number of GT dinucleotide repeats in the gene promoter. Here, among cohorts in areas of Taiwan affected by endemic arsenic poisoning, individuals who were homozygous for short (GT)n polymorphisms (S/S, <27 dinucleotide repeats) were found to be at increased risk of skin cancer and lung squamous cell carcinoma. Arsenic exposure further increased skin cancer risk among S/S individuals. All S‐allele carriers, however, had a reduced risk of lung adenocarcinoma, a malignancy unrelated to arsenic exposure.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>26566708</pmid><doi>10.1002/ijc.29926</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Arsenic arsenic exposure Arsenic Poisoning - complications Arsenic Poisoning - epidemiology Arsenic Poisoning - genetics Bowen's disease Cancer cancer risk Drinking Water - adverse effects Endemic Diseases Female Fluorescent Antibody Technique genetic polymorphism Genetic Predisposition to Disease - genetics Genotype Genotype & phenotype Heme Oxygenase-1 - genetics heme oxygenase‐1 Histology Humans Incidence Lung cancer Male Medical research Middle Aged Neoplasms - chemically induced Neoplasms - enzymology Neoplasms - genetics Polymorphism Polymorphism, Single Nucleotide Promoter Regions, Genetic - genetics Proportional Hazards Models Prospective Studies Reverse Transcriptase Polymerase Chain Reaction Risk factors Taiwan - epidemiology |
| title | Effect of heme oxygenase‐1 gene promoter polymorphism on cancer risk by histological subtype: A prospective study in arseniasis‐endemic areas in Taiwan |
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