Association between polymorphisms of EPHX1 and XRCC1 genes and the risk of childhood acute lymphoblastic leukemia
Microsomal epoxide hydrolase, EPHX1, plays a central role in the detoxification of potentially genotoxic epoxide intermediates. In this study, we firstly aimed to investigate the relationship between EPHX1 Tyr113His and His139Arg variants, and the risk of incidence of childhood acute lymphoblastic l...
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| Veröffentlicht in: | Archives of toxicology 2012-03, Vol.86 (3), p.431-439 |
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| description | Microsomal epoxide hydrolase, EPHX1, plays a central role in the detoxification of potentially genotoxic epoxide intermediates. In this study, we firstly aimed to investigate the relationship between
EPHX1
Tyr113His and His139Arg variants, and the risk of incidence of childhood acute lymphoblastic leukemia (ALL) in Turkish population, comprised of 190 healthy controls and 167 ALL patients. In exon 3 Tyr113His polymorphism, 113His/His homozygous mutant genotype with slow activity was 18.6% in ALL patients and 9% in controls, indicating 113His/His slow activity genotype was significantly associated with an increased risk of childhood ALL (OR: 2.3, 95% CI, 1.2–4.4,
P
= 0.01). No significant association was found between exon 4 His139Arg variant and the risk of ALL. When both exon 3 Tyr113His and exon 4 His139Arg polymorphisms were considered together, only the exon 3 113His/His, homozygous mutant, slow activity genotype with exon 4 wild-type genotype 139His/His was significantly increased the risk of ALL 2.4-fold (OR: 2.4,
P
= 0.02). We also evaluated whether haplotype analysis for
EPHX1
Tyr113His polymorphism together with DNA protein XRCC1 Arg399Gln variant known for its deficient DNA repair capacity would represent more prominent risk factors for the development of childhood ALL. Accordingly, the co-presence of Tyr113His variant of
EPHX1
and Arg399Gln variant of
XRCC1
in the same individuals significantly increased the risk of childhood ALL up to 2.1-fold (OR = 2.1,
P
= 0.03). Moreover, homozygous mutant genotype for both genes significantly and considerably increased the risk of childhood ALL 8.5-fold (OR: 8.5,
P
= 0.03). In conclusion, individuals with
EPHX1
113His/His slow activity genotype may not detoxify reactive carcinogenic epoxides efficiently, binding of reactive epoxides to DNA cause DNA damage. With the inadequate polymorphic DNA repair protein, XRCC1, this situation ultimately leads to significantly increased susceptibility for childhood ALL. |
| doi_str_mv | 10.1007/s00204-011-0760-8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_926903800</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2590744141</sourcerecordid><originalsourceid>FETCH-LOGICAL-c402t-ed17e9497339ce31687e8203a0face4d7926209c21c2f96fe1dd2782a5354dad3</originalsourceid><addsrcrecordid>eNp1kV9LHTEQxUNR6q3tB-iLBF_6tHWS7J_kUS5WBaFSWvAt5CazbnR3sya7iN_e3F5rQfBpGOZ3zgxzCPnK4DsDaE4SAIeyAMYKaGoo5AeyYqXguRNyj6xAlFBUTc0OyKeU7gAYl0p8JAecKSmkrFfk4TSlYL2ZfRjpBudHxJFOoX8aQpw6n4ZEQ0vPri9uGDWjoze_1mtGb3HE9LefO6TRp_stZTvfuy4ER41dZqTZZOrCpjdp9pb2uNzj4M1nst-aPuGXl3pI_vw4-72-KK5-nl-uT68KWwKfC3SsQVWqRghlUbBaNig5CAOtsVi6RvGag7KcWd6qukXmHG8kN5WoSmecOCTfdr5TDA8LplkPPlnsezNiWJLOegVCAmTy-A15F5Y45uMyxEXNqkpmiO0gG0NKEVs9RT-Y-KQZ6G0aepeGzmnobRp6qzl6MV42A7pXxb_3Z4DvgJRH4y3G_5vfd30GAYuUZQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>922361558</pqid></control><display><type>article</type><title>Association between polymorphisms of EPHX1 and XRCC1 genes and the risk of childhood acute lymphoblastic leukemia</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Tumer, Tugba Boyunegmez ; Sahin, Gurses ; Arinç, Emel</creator><creatorcontrib>Tumer, Tugba Boyunegmez ; Sahin, Gurses ; Arinç, Emel</creatorcontrib><description>Microsomal epoxide hydrolase, EPHX1, plays a central role in the detoxification of potentially genotoxic epoxide intermediates. In this study, we firstly aimed to investigate the relationship between
EPHX1
Tyr113His and His139Arg variants, and the risk of incidence of childhood acute lymphoblastic leukemia (ALL) in Turkish population, comprised of 190 healthy controls and 167 ALL patients. In exon 3 Tyr113His polymorphism, 113His/His homozygous mutant genotype with slow activity was 18.6% in ALL patients and 9% in controls, indicating 113His/His slow activity genotype was significantly associated with an increased risk of childhood ALL (OR: 2.3, 95% CI, 1.2–4.4,
P
= 0.01). No significant association was found between exon 4 His139Arg variant and the risk of ALL. When both exon 3 Tyr113His and exon 4 His139Arg polymorphisms were considered together, only the exon 3 113His/His, homozygous mutant, slow activity genotype with exon 4 wild-type genotype 139His/His was significantly increased the risk of ALL 2.4-fold (OR: 2.4,
P
= 0.02). We also evaluated whether haplotype analysis for
EPHX1
Tyr113His polymorphism together with DNA protein XRCC1 Arg399Gln variant known for its deficient DNA repair capacity would represent more prominent risk factors for the development of childhood ALL. Accordingly, the co-presence of Tyr113His variant of
EPHX1
and Arg399Gln variant of
XRCC1
in the same individuals significantly increased the risk of childhood ALL up to 2.1-fold (OR = 2.1,
P
= 0.03). Moreover, homozygous mutant genotype for both genes significantly and considerably increased the risk of childhood ALL 8.5-fold (OR: 8.5,
P
= 0.03). In conclusion, individuals with
EPHX1
113His/His slow activity genotype may not detoxify reactive carcinogenic epoxides efficiently, binding of reactive epoxides to DNA cause DNA damage. With the inadequate polymorphic DNA repair protein, XRCC1, this situation ultimately leads to significantly increased susceptibility for childhood ALL.</description><identifier>ISSN: 0340-5761</identifier><identifier>EISSN: 1432-0738</identifier><identifier>DOI: 10.1007/s00204-011-0760-8</identifier><identifier>PMID: 21983886</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Adolescent ; Adult ; Aged ; Biomedical and Life Sciences ; Biomedicine ; Child ; Child, Preschool ; DNA-Binding Proteins - genetics ; Environmental Health ; Epoxide Hydrolases - genetics ; Female ; Genes ; Genetic Predisposition to Disease ; Genotype ; Humans ; Infant ; Leukemia ; Lymphoma ; Male ; Middle Aged ; Occupational Medicine/Industrial Medicine ; Pharmacology/Toxicology ; Polymorphism ; Polymorphism, Genetic ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics ; Risk Factors ; Toxicogenomics ; X-ray Repair Cross Complementing Protein 1</subject><ispartof>Archives of toxicology, 2012-03, Vol.86 (3), p.431-439</ispartof><rights>Springer-Verlag 2011</rights><rights>Springer-Verlag 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c402t-ed17e9497339ce31687e8203a0face4d7926209c21c2f96fe1dd2782a5354dad3</citedby><cites>FETCH-LOGICAL-c402t-ed17e9497339ce31687e8203a0face4d7926209c21c2f96fe1dd2782a5354dad3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00204-011-0760-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00204-011-0760-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21983886$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tumer, Tugba Boyunegmez</creatorcontrib><creatorcontrib>Sahin, Gurses</creatorcontrib><creatorcontrib>Arinç, Emel</creatorcontrib><title>Association between polymorphisms of EPHX1 and XRCC1 genes and the risk of childhood acute lymphoblastic leukemia</title><title>Archives of toxicology</title><addtitle>Arch Toxicol</addtitle><addtitle>Arch Toxicol</addtitle><description>Microsomal epoxide hydrolase, EPHX1, plays a central role in the detoxification of potentially genotoxic epoxide intermediates. In this study, we firstly aimed to investigate the relationship between
EPHX1
Tyr113His and His139Arg variants, and the risk of incidence of childhood acute lymphoblastic leukemia (ALL) in Turkish population, comprised of 190 healthy controls and 167 ALL patients. In exon 3 Tyr113His polymorphism, 113His/His homozygous mutant genotype with slow activity was 18.6% in ALL patients and 9% in controls, indicating 113His/His slow activity genotype was significantly associated with an increased risk of childhood ALL (OR: 2.3, 95% CI, 1.2–4.4,
P
= 0.01). No significant association was found between exon 4 His139Arg variant and the risk of ALL. When both exon 3 Tyr113His and exon 4 His139Arg polymorphisms were considered together, only the exon 3 113His/His, homozygous mutant, slow activity genotype with exon 4 wild-type genotype 139His/His was significantly increased the risk of ALL 2.4-fold (OR: 2.4,
P
= 0.02). We also evaluated whether haplotype analysis for
EPHX1
Tyr113His polymorphism together with DNA protein XRCC1 Arg399Gln variant known for its deficient DNA repair capacity would represent more prominent risk factors for the development of childhood ALL. Accordingly, the co-presence of Tyr113His variant of
EPHX1
and Arg399Gln variant of
XRCC1
in the same individuals significantly increased the risk of childhood ALL up to 2.1-fold (OR = 2.1,
P
= 0.03). Moreover, homozygous mutant genotype for both genes significantly and considerably increased the risk of childhood ALL 8.5-fold (OR: 8.5,
P
= 0.03). In conclusion, individuals with
EPHX1
113His/His slow activity genotype may not detoxify reactive carcinogenic epoxides efficiently, binding of reactive epoxides to DNA cause DNA damage. With the inadequate polymorphic DNA repair protein, XRCC1, this situation ultimately leads to significantly increased susceptibility for childhood ALL.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Environmental Health</subject><subject>Epoxide Hydrolases - genetics</subject><subject>Female</subject><subject>Genes</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Humans</subject><subject>Infant</subject><subject>Leukemia</subject><subject>Lymphoma</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Occupational Medicine/Industrial Medicine</subject><subject>Pharmacology/Toxicology</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics</subject><subject>Risk Factors</subject><subject>Toxicogenomics</subject><subject>X-ray Repair Cross Complementing Protein 1</subject><issn>0340-5761</issn><issn>1432-0738</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kV9LHTEQxUNR6q3tB-iLBF_6tHWS7J_kUS5WBaFSWvAt5CazbnR3sya7iN_e3F5rQfBpGOZ3zgxzCPnK4DsDaE4SAIeyAMYKaGoo5AeyYqXguRNyj6xAlFBUTc0OyKeU7gAYl0p8JAecKSmkrFfk4TSlYL2ZfRjpBudHxJFOoX8aQpw6n4ZEQ0vPri9uGDWjoze_1mtGb3HE9LefO6TRp_stZTvfuy4ER41dZqTZZOrCpjdp9pb2uNzj4M1nst-aPuGXl3pI_vw4-72-KK5-nl-uT68KWwKfC3SsQVWqRghlUbBaNig5CAOtsVi6RvGag7KcWd6qukXmHG8kN5WoSmecOCTfdr5TDA8LplkPPlnsezNiWJLOegVCAmTy-A15F5Y45uMyxEXNqkpmiO0gG0NKEVs9RT-Y-KQZ6G0aepeGzmnobRp6qzl6MV42A7pXxb_3Z4DvgJRH4y3G_5vfd30GAYuUZQ</recordid><startdate>20120301</startdate><enddate>20120301</enddate><creator>Tumer, Tugba Boyunegmez</creator><creator>Sahin, Gurses</creator><creator>Arinç, Emel</creator><general>Springer-Verlag</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7T2</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20120301</creationdate><title>Association between polymorphisms of EPHX1 and XRCC1 genes and the risk of childhood acute lymphoblastic leukemia</title><author>Tumer, Tugba Boyunegmez ; Sahin, Gurses ; Arinç, Emel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c402t-ed17e9497339ce31687e8203a0face4d7926209c21c2f96fe1dd2782a5354dad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Environmental Health</topic><topic>Epoxide Hydrolases - genetics</topic><topic>Female</topic><topic>Genes</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Humans</topic><topic>Infant</topic><topic>Leukemia</topic><topic>Lymphoma</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Occupational Medicine/Industrial Medicine</topic><topic>Pharmacology/Toxicology</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics</topic><topic>Risk Factors</topic><topic>Toxicogenomics</topic><topic>X-ray Repair Cross Complementing Protein 1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tumer, Tugba Boyunegmez</creatorcontrib><creatorcontrib>Sahin, Gurses</creatorcontrib><creatorcontrib>Arinç, Emel</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health and Safety Science Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Research Library (Corporate)</collection><collection>Environmental Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Environmental Science Collection</collection><collection>ProQuest Central Basic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Archives of toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tumer, Tugba Boyunegmez</au><au>Sahin, Gurses</au><au>Arinç, Emel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association between polymorphisms of EPHX1 and XRCC1 genes and the risk of childhood acute lymphoblastic leukemia</atitle><jtitle>Archives of toxicology</jtitle><stitle>Arch Toxicol</stitle><addtitle>Arch Toxicol</addtitle><date>2012-03-01</date><risdate>2012</risdate><volume>86</volume><issue>3</issue><spage>431</spage><epage>439</epage><pages>431-439</pages><issn>0340-5761</issn><eissn>1432-0738</eissn><abstract>Microsomal epoxide hydrolase, EPHX1, plays a central role in the detoxification of potentially genotoxic epoxide intermediates. In this study, we firstly aimed to investigate the relationship between
EPHX1
Tyr113His and His139Arg variants, and the risk of incidence of childhood acute lymphoblastic leukemia (ALL) in Turkish population, comprised of 190 healthy controls and 167 ALL patients. In exon 3 Tyr113His polymorphism, 113His/His homozygous mutant genotype with slow activity was 18.6% in ALL patients and 9% in controls, indicating 113His/His slow activity genotype was significantly associated with an increased risk of childhood ALL (OR: 2.3, 95% CI, 1.2–4.4,
P
= 0.01). No significant association was found between exon 4 His139Arg variant and the risk of ALL. When both exon 3 Tyr113His and exon 4 His139Arg polymorphisms were considered together, only the exon 3 113His/His, homozygous mutant, slow activity genotype with exon 4 wild-type genotype 139His/His was significantly increased the risk of ALL 2.4-fold (OR: 2.4,
P
= 0.02). We also evaluated whether haplotype analysis for
EPHX1
Tyr113His polymorphism together with DNA protein XRCC1 Arg399Gln variant known for its deficient DNA repair capacity would represent more prominent risk factors for the development of childhood ALL. Accordingly, the co-presence of Tyr113His variant of
EPHX1
and Arg399Gln variant of
XRCC1
in the same individuals significantly increased the risk of childhood ALL up to 2.1-fold (OR = 2.1,
P
= 0.03). Moreover, homozygous mutant genotype for both genes significantly and considerably increased the risk of childhood ALL 8.5-fold (OR: 8.5,
P
= 0.03). In conclusion, individuals with
EPHX1
113His/His slow activity genotype may not detoxify reactive carcinogenic epoxides efficiently, binding of reactive epoxides to DNA cause DNA damage. With the inadequate polymorphic DNA repair protein, XRCC1, this situation ultimately leads to significantly increased susceptibility for childhood ALL.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>21983886</pmid><doi>10.1007/s00204-011-0760-8</doi><tpages>9</tpages></addata></record> |
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| identifier | ISSN: 0340-5761 |
| ispartof | Archives of toxicology, 2012-03, Vol.86 (3), p.431-439 |
| issn | 0340-5761 1432-0738 |
| language | eng |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Adolescent Adult Aged Biomedical and Life Sciences Biomedicine Child Child, Preschool DNA-Binding Proteins - genetics Environmental Health Epoxide Hydrolases - genetics Female Genes Genetic Predisposition to Disease Genotype Humans Infant Leukemia Lymphoma Male Middle Aged Occupational Medicine/Industrial Medicine Pharmacology/Toxicology Polymorphism Polymorphism, Genetic Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics Risk Factors Toxicogenomics X-ray Repair Cross Complementing Protein 1 |
| title | Association between polymorphisms of EPHX1 and XRCC1 genes and the risk of childhood acute lymphoblastic leukemia |
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