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NAD(P)H:quinone oxidoreductase 1 null genotype is not associated with pediatric de novo acute leukemia
Background NAD(P)H:quinone oxidoreductase1 (NQO1) is a two‐electron reductase that detoxifies quinones derived from the oxidation of phenolic metabolites of benzene. Exposure to benzene metabolites increases the risk of hematotoxicity and leukemia. NQO1 enzyme activity protects the cells against met...
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Published in: | Pediatric Blood & Cancer 2004-10, Vol.43 (5), p.568-570 |
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container_title | Pediatric Blood & Cancer |
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creator | Sirma, Sema Agaoglu, Leyla Yildiz, Inci Cayli, Dilara Horgusluoglu, Emrin Anak, Sema Yuksel, Lebriz Unuvar, Aysegul Celkan, Tiraje Apak, Hilmi Karakas, Zeynep Devecioglu, Omer Ozbek, Ugur |
description | Background
NAD(P)H:quinone oxidoreductase1 (NQO1) is a two‐electron reductase that detoxifies quinones derived from the oxidation of phenolic metabolites of benzene. Exposure to benzene metabolites increases the risk of hematotoxicity and leukemia. NQO1 enzyme activity protects the cells against metabolites of benzene. C to T base substitution at nucleotide 609 of NQO1 cDNA (C609T) results in loss of enzyme activity. Low NQO1 activity may play a role in etiology of acute leukemia.
Procedure
We analyzed NQO1 C609T gene polymorphism using the PCR‐RFLP method in 273 patients with de novo acute leukemia (189 acute lymphoblastic leukemia (ALL), and 84 acute myeloid leukemia (AML) and 286 healthy volunteers to investigate the role of NQO1 polymorphism in the etiology of acute leukemia.
Results and Conclusions
The frequency of homozygosity for NOQ1 C609T polymorphism was 3.5% in the healthy control population and 2.5% in pediatric acute leukemia. The NQO1 C609T allele frequency was not statistically different in the children with acute leukemia in comparison to the controls (odds ratio (OR), 0.76; 95% confidence interval (CI), 0.58–1.01; P = 0.06). The distribution of NQO1 genotypes among children with acute leukemia was not statistically different from the control group (P = 0.13). These findings do not support the role of NQO1 C609T polymorphism in the etiology of de novo pediatric acute leukemia. © 2004 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/pbc.20098 |
format | article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_66903529</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>20610436</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4208-80dc4bf2983fb23264f341dd90ec87daa9bba7381fd84fb7124115c53d5b60833</originalsourceid><addsrcrecordid>eNqF0M9PFTEQB_DGaATRg_-A6UUjh4X-2Ha73PChDwNBDhqPTbedamXfdml3gfffW3xPOBlPM5N8Zib5IvSakgNKCDscO3vACGnVE7RLRS0qQWjz9KEn7Q56kfOvQiUR6jnaoYIrxpp6F_mL45P3l_unR9dzGOIAON4FFxO42U4mA6Z4mPse_4AhTusRcMi4dNjkHG0wEzh8G6afeARXphQsdlDATcTGzhPgHuYrWAXzEj3zps_walv30LdPH78uTqvzL8vPi-PzytaMqEoRZ-vOs1Zx3zHOZO15TZ1rCVjVOGParjMNV9Q7VfuuoaymVFjBnegkUZzvoXebu2OK1zPkSa9CttD3ZoA4Zy1lS7hg7X8hI5KSmssC9zfQpphzAq_HFFYmrTUl-j59XdLXf9Iv9s326NytwD3KbdwFvN0Ck63pfTKDDfnRSdoozu7d4cbdhh7W__6oLz8s_r6uNhshT3D3sGHSlZYNb4T-frHUy7OSHSdnmvPfUhupiA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>20610436</pqid></control><display><type>article</type><title>NAD(P)H:quinone oxidoreductase 1 null genotype is not associated with pediatric de novo acute leukemia</title><source>Wiley</source><creator>Sirma, Sema ; Agaoglu, Leyla ; Yildiz, Inci ; Cayli, Dilara ; Horgusluoglu, Emrin ; Anak, Sema ; Yuksel, Lebriz ; Unuvar, Aysegul ; Celkan, Tiraje ; Apak, Hilmi ; Karakas, Zeynep ; Devecioglu, Omer ; Ozbek, Ugur</creator><creatorcontrib>Sirma, Sema ; Agaoglu, Leyla ; Yildiz, Inci ; Cayli, Dilara ; Horgusluoglu, Emrin ; Anak, Sema ; Yuksel, Lebriz ; Unuvar, Aysegul ; Celkan, Tiraje ; Apak, Hilmi ; Karakas, Zeynep ; Devecioglu, Omer ; Ozbek, Ugur</creatorcontrib><description>Background
NAD(P)H:quinone oxidoreductase1 (NQO1) is a two‐electron reductase that detoxifies quinones derived from the oxidation of phenolic metabolites of benzene. Exposure to benzene metabolites increases the risk of hematotoxicity and leukemia. NQO1 enzyme activity protects the cells against metabolites of benzene. C to T base substitution at nucleotide 609 of NQO1 cDNA (C609T) results in loss of enzyme activity. Low NQO1 activity may play a role in etiology of acute leukemia.
Procedure
We analyzed NQO1 C609T gene polymorphism using the PCR‐RFLP method in 273 patients with de novo acute leukemia (189 acute lymphoblastic leukemia (ALL), and 84 acute myeloid leukemia (AML) and 286 healthy volunteers to investigate the role of NQO1 polymorphism in the etiology of acute leukemia.
Results and Conclusions
The frequency of homozygosity for NOQ1 C609T polymorphism was 3.5% in the healthy control population and 2.5% in pediatric acute leukemia. The NQO1 C609T allele frequency was not statistically different in the children with acute leukemia in comparison to the controls (odds ratio (OR), 0.76; 95% confidence interval (CI), 0.58–1.01; P = 0.06). The distribution of NQO1 genotypes among children with acute leukemia was not statistically different from the control group (P = 0.13). These findings do not support the role of NQO1 C609T polymorphism in the etiology of de novo pediatric acute leukemia. © 2004 Wiley‐Liss, Inc.</description><identifier>ISSN: 1545-5009</identifier><identifier>EISSN: 1545-5017</identifier><identifier>EISSN: 1096-911X</identifier><identifier>DOI: 10.1002/pbc.20098</identifier><identifier>PMID: 15382274</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Acute Disease ; acute leukemia risk ; Adolescent ; Biological and medical sciences ; Child ; Child, Preschool ; Female ; General aspects ; Genotype ; Humans ; Infant ; Leukemia, Myeloid - etiology ; Leukemia, Myeloid - genetics ; Male ; Medical sciences ; NAD(P)H Dehydrogenase (Quinone) - genetics ; NQO1 gene polymorphism ; pediatric acute leukemia ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics ; Tumors</subject><ispartof>Pediatric Blood & Cancer, 2004-10, Vol.43 (5), p.568-570</ispartof><rights>Copyright © 2004 Wiley‐Liss, Inc.</rights><rights>2004 INIST-CNRS</rights><rights>Copyright 2004 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4208-80dc4bf2983fb23264f341dd90ec87daa9bba7381fd84fb7124115c53d5b60833</citedby><cites>FETCH-LOGICAL-c4208-80dc4bf2983fb23264f341dd90ec87daa9bba7381fd84fb7124115c53d5b60833</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16178324$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15382274$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sirma, Sema</creatorcontrib><creatorcontrib>Agaoglu, Leyla</creatorcontrib><creatorcontrib>Yildiz, Inci</creatorcontrib><creatorcontrib>Cayli, Dilara</creatorcontrib><creatorcontrib>Horgusluoglu, Emrin</creatorcontrib><creatorcontrib>Anak, Sema</creatorcontrib><creatorcontrib>Yuksel, Lebriz</creatorcontrib><creatorcontrib>Unuvar, Aysegul</creatorcontrib><creatorcontrib>Celkan, Tiraje</creatorcontrib><creatorcontrib>Apak, Hilmi</creatorcontrib><creatorcontrib>Karakas, Zeynep</creatorcontrib><creatorcontrib>Devecioglu, Omer</creatorcontrib><creatorcontrib>Ozbek, Ugur</creatorcontrib><title>NAD(P)H:quinone oxidoreductase 1 null genotype is not associated with pediatric de novo acute leukemia</title><title>Pediatric Blood & Cancer</title><addtitle>Pediatr. Blood Cancer</addtitle><description>Background
NAD(P)H:quinone oxidoreductase1 (NQO1) is a two‐electron reductase that detoxifies quinones derived from the oxidation of phenolic metabolites of benzene. Exposure to benzene metabolites increases the risk of hematotoxicity and leukemia. NQO1 enzyme activity protects the cells against metabolites of benzene. C to T base substitution at nucleotide 609 of NQO1 cDNA (C609T) results in loss of enzyme activity. Low NQO1 activity may play a role in etiology of acute leukemia.
Procedure
We analyzed NQO1 C609T gene polymorphism using the PCR‐RFLP method in 273 patients with de novo acute leukemia (189 acute lymphoblastic leukemia (ALL), and 84 acute myeloid leukemia (AML) and 286 healthy volunteers to investigate the role of NQO1 polymorphism in the etiology of acute leukemia.
Results and Conclusions
The frequency of homozygosity for NOQ1 C609T polymorphism was 3.5% in the healthy control population and 2.5% in pediatric acute leukemia. The NQO1 C609T allele frequency was not statistically different in the children with acute leukemia in comparison to the controls (odds ratio (OR), 0.76; 95% confidence interval (CI), 0.58–1.01; P = 0.06). The distribution of NQO1 genotypes among children with acute leukemia was not statistically different from the control group (P = 0.13). These findings do not support the role of NQO1 C609T polymorphism in the etiology of de novo pediatric acute leukemia. © 2004 Wiley‐Liss, Inc.</description><subject>Acute Disease</subject><subject>acute leukemia risk</subject><subject>Adolescent</subject><subject>Biological and medical sciences</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Female</subject><subject>General aspects</subject><subject>Genotype</subject><subject>Humans</subject><subject>Infant</subject><subject>Leukemia, Myeloid - etiology</subject><subject>Leukemia, Myeloid - genetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>NAD(P)H Dehydrogenase (Quinone) - genetics</subject><subject>NQO1 gene polymorphism</subject><subject>pediatric acute leukemia</subject><subject>Polymerase Chain Reaction</subject><subject>Polymorphism, Genetic</subject><subject>Polymorphism, Restriction Fragment Length</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics</subject><subject>Tumors</subject><issn>1545-5009</issn><issn>1545-5017</issn><issn>1096-911X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNqF0M9PFTEQB_DGaATRg_-A6UUjh4X-2Ha73PChDwNBDhqPTbedamXfdml3gfffW3xPOBlPM5N8Zib5IvSakgNKCDscO3vACGnVE7RLRS0qQWjz9KEn7Q56kfOvQiUR6jnaoYIrxpp6F_mL45P3l_unR9dzGOIAON4FFxO42U4mA6Z4mPse_4AhTusRcMi4dNjkHG0wEzh8G6afeARXphQsdlDATcTGzhPgHuYrWAXzEj3zps_walv30LdPH78uTqvzL8vPi-PzytaMqEoRZ-vOs1Zx3zHOZO15TZ1rCVjVOGParjMNV9Q7VfuuoaymVFjBnegkUZzvoXebu2OK1zPkSa9CttD3ZoA4Zy1lS7hg7X8hI5KSmssC9zfQpphzAq_HFFYmrTUl-j59XdLXf9Iv9s326NytwD3KbdwFvN0Ck63pfTKDDfnRSdoozu7d4cbdhh7W__6oLz8s_r6uNhshT3D3sGHSlZYNb4T-frHUy7OSHSdnmvPfUhupiA</recordid><startdate>200410</startdate><enddate>200410</enddate><creator>Sirma, Sema</creator><creator>Agaoglu, Leyla</creator><creator>Yildiz, Inci</creator><creator>Cayli, Dilara</creator><creator>Horgusluoglu, Emrin</creator><creator>Anak, Sema</creator><creator>Yuksel, Lebriz</creator><creator>Unuvar, Aysegul</creator><creator>Celkan, Tiraje</creator><creator>Apak, Hilmi</creator><creator>Karakas, Zeynep</creator><creator>Devecioglu, Omer</creator><creator>Ozbek, Ugur</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</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>H94</scope><scope>7X8</scope></search><sort><creationdate>200410</creationdate><title>NAD(P)H:quinone oxidoreductase 1 null genotype is not associated with pediatric de novo acute leukemia</title><author>Sirma, Sema ; Agaoglu, Leyla ; Yildiz, Inci ; Cayli, Dilara ; Horgusluoglu, Emrin ; Anak, Sema ; Yuksel, Lebriz ; Unuvar, Aysegul ; Celkan, Tiraje ; Apak, Hilmi ; Karakas, Zeynep ; Devecioglu, Omer ; Ozbek, Ugur</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4208-80dc4bf2983fb23264f341dd90ec87daa9bba7381fd84fb7124115c53d5b60833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Acute Disease</topic><topic>acute leukemia risk</topic><topic>Adolescent</topic><topic>Biological and medical sciences</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Female</topic><topic>General aspects</topic><topic>Genotype</topic><topic>Humans</topic><topic>Infant</topic><topic>Leukemia, Myeloid - etiology</topic><topic>Leukemia, Myeloid - genetics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>NAD(P)H Dehydrogenase (Quinone) - genetics</topic><topic>NQO1 gene polymorphism</topic><topic>pediatric acute leukemia</topic><topic>Polymerase Chain Reaction</topic><topic>Polymorphism, Genetic</topic><topic>Polymorphism, Restriction Fragment Length</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sirma, Sema</creatorcontrib><creatorcontrib>Agaoglu, Leyla</creatorcontrib><creatorcontrib>Yildiz, Inci</creatorcontrib><creatorcontrib>Cayli, Dilara</creatorcontrib><creatorcontrib>Horgusluoglu, Emrin</creatorcontrib><creatorcontrib>Anak, Sema</creatorcontrib><creatorcontrib>Yuksel, Lebriz</creatorcontrib><creatorcontrib>Unuvar, Aysegul</creatorcontrib><creatorcontrib>Celkan, Tiraje</creatorcontrib><creatorcontrib>Apak, Hilmi</creatorcontrib><creatorcontrib>Karakas, Zeynep</creatorcontrib><creatorcontrib>Devecioglu, Omer</creatorcontrib><creatorcontrib>Ozbek, Ugur</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>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Pediatric Blood & Cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sirma, Sema</au><au>Agaoglu, Leyla</au><au>Yildiz, Inci</au><au>Cayli, Dilara</au><au>Horgusluoglu, Emrin</au><au>Anak, Sema</au><au>Yuksel, Lebriz</au><au>Unuvar, Aysegul</au><au>Celkan, Tiraje</au><au>Apak, Hilmi</au><au>Karakas, Zeynep</au><au>Devecioglu, Omer</au><au>Ozbek, Ugur</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>NAD(P)H:quinone oxidoreductase 1 null genotype is not associated with pediatric de novo acute leukemia</atitle><jtitle>Pediatric Blood & Cancer</jtitle><addtitle>Pediatr. Blood Cancer</addtitle><date>2004-10</date><risdate>2004</risdate><volume>43</volume><issue>5</issue><spage>568</spage><epage>570</epage><pages>568-570</pages><issn>1545-5009</issn><eissn>1545-5017</eissn><eissn>1096-911X</eissn><abstract>Background
NAD(P)H:quinone oxidoreductase1 (NQO1) is a two‐electron reductase that detoxifies quinones derived from the oxidation of phenolic metabolites of benzene. Exposure to benzene metabolites increases the risk of hematotoxicity and leukemia. NQO1 enzyme activity protects the cells against metabolites of benzene. C to T base substitution at nucleotide 609 of NQO1 cDNA (C609T) results in loss of enzyme activity. Low NQO1 activity may play a role in etiology of acute leukemia.
Procedure
We analyzed NQO1 C609T gene polymorphism using the PCR‐RFLP method in 273 patients with de novo acute leukemia (189 acute lymphoblastic leukemia (ALL), and 84 acute myeloid leukemia (AML) and 286 healthy volunteers to investigate the role of NQO1 polymorphism in the etiology of acute leukemia.
Results and Conclusions
The frequency of homozygosity for NOQ1 C609T polymorphism was 3.5% in the healthy control population and 2.5% in pediatric acute leukemia. The NQO1 C609T allele frequency was not statistically different in the children with acute leukemia in comparison to the controls (odds ratio (OR), 0.76; 95% confidence interval (CI), 0.58–1.01; P = 0.06). The distribution of NQO1 genotypes among children with acute leukemia was not statistically different from the control group (P = 0.13). These findings do not support the role of NQO1 C609T polymorphism in the etiology of de novo pediatric acute leukemia. © 2004 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>15382274</pmid><doi>10.1002/pbc.20098</doi><tpages>3</tpages></addata></record> |
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subjects | Acute Disease acute leukemia risk Adolescent Biological and medical sciences Child Child, Preschool Female General aspects Genotype Humans Infant Leukemia, Myeloid - etiology Leukemia, Myeloid - genetics Male Medical sciences NAD(P)H Dehydrogenase (Quinone) - genetics NQO1 gene polymorphism pediatric acute leukemia Polymerase Chain Reaction Polymorphism, Genetic Polymorphism, Restriction Fragment Length Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics Tumors |
title | NAD(P)H:quinone oxidoreductase 1 null genotype is not associated with pediatric de novo acute leukemia |
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