Loading…

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...

Full description

Saved in:
Bibliographic Details
Published in:Pediatric Blood & Cancer 2004-10, Vol.43 (5), p.568-570
Main Authors: 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
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c4208-80dc4bf2983fb23264f341dd90ec87daa9bba7381fd84fb7124115c53d5b60833
cites cdi_FETCH-LOGICAL-c4208-80dc4bf2983fb23264f341dd90ec87daa9bba7381fd84fb7124115c53d5b60833
container_end_page 570
container_issue 5
container_start_page 568
container_title Pediatric Blood & Cancer
container_volume 43
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 &amp; 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&amp;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 &amp; 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 &amp; 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 &amp; 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>
fulltext fulltext
identifier ISSN: 1545-5009
ispartof Pediatric Blood & Cancer, 2004-10, Vol.43 (5), p.568-570
issn 1545-5009
1545-5017
1096-911X
language eng
recordid cdi_proquest_miscellaneous_66903529
source Wiley
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
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T11%3A23%3A30IST&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=NAD(P)H:quinone%20oxidoreductase%201%20null%20genotype%20is%20not%20associated%20with%20pediatric%20de%20novo%20acute%20leukemia&rft.jtitle=Pediatric%20Blood%20&%20Cancer&rft.au=Sirma,%20Sema&rft.date=2004-10&rft.volume=43&rft.issue=5&rft.spage=568&rft.epage=570&rft.pages=568-570&rft.issn=1545-5009&rft.eissn=1545-5017&rft_id=info:doi/10.1002/pbc.20098&rft_dat=%3Cproquest_cross%3E20610436%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c4208-80dc4bf2983fb23264f341dd90ec87daa9bba7381fd84fb7124115c53d5b60833%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=20610436&rft_id=info:pmid/15382274&rfr_iscdi=true