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dc.contributor.CRUESPUniversidade Estadual de Campinaspt_BR
dc.typeArtigo de periódicopt_BR
dc.titleIncreased risk for acute myeloid leukaemia in individuals with glutathione S-transferase mu 1 (GSTM1) and theta 1 (GSTT1) gene defectspt_BR
dc.contributor.authorArruda, VRpt_BR
dc.contributor.authorLima, CSPpt_BR
dc.contributor.authorGrignoli, CREpt_BR
dc.contributor.authorde Melo, MBpt_BR
dc.contributor.authorLorand-Metze, Ipt_BR
dc.contributor.authorAlberto, FLpt_BR
dc.contributor.authorSaad, STOpt_BR
dc.contributor.authorCosta, FFpt_BR
unicamp.authorState Univ Campinas, Dept Internal Med, Campinas, SP, Brazilpt_BR
dc.subjectglutathione S-transferasept_BR
dc.subjectcarcinogenpt_BR
dc.subjectacute myeloid leukaemiapt_BR
dc.subjectmyelodysplastic syndromept_BR
dc.subjectaplastic anaemiapt_BR
dc.subject.wosAcute Lymphoblastic-leukemiapt_BR
dc.subject.wosMyelodysplastic Syndromespt_BR
dc.subject.wosEnvironmental Carcinogenesispt_BR
dc.subject.wosCancer Susceptibilitypt_BR
dc.subject.wosAplastic-anemiapt_BR
dc.subject.wosExposurept_BR
dc.subject.wosGenotypespt_BR
dc.subject.wosBenzenept_BR
dc.subject.wosPolymorphismspt_BR
dc.subject.wosChildrenpt_BR
dc.description.abstractObjectives: Glutathione S-transferases (GST) modulate the effects of exposure to various cytotoxic and genotoxic agents, including those associated with increased risks of the myelodysplastic syndrome (MDS), acute myeloid leukaemia (AML) and aplastic anemia (AA). Both the GST mu 1 (GSTM1) and GST theta 1 (GSTT1) genes have a null variant allele in which the entire gene is absent. In this study, we tested whether null genotypes for the GSTM1 and GSTT1 genes altered the risks for MDS, AML and AA. Methods: Genomic DNA from 49 MDS, 38 AML and 37 AA patients and 276 controls was analysed using the polymerase chain reaction (PCR). Results: The frequencies of GSTM1 (73.6%) and GSTT1 (34.2%) null genotypes were significantly higher in AML patients than in the controls (36.9 and 18.1%, respectively). A higher frequency of the combined null genotype for both genes was also observed in patients with AML (26.3% compared with 5.0% in the controls). In contrast, no differences in the frequencies of the null genotypes were found among MDS patients, AA patients and the controls. Conclusion: Our observation of a 4.7-fold (95% CI: 2.1-11.0) and 2.3-fold (95% CI: 1.0-5.2) increased risk associated with the GSTM1 and GSTT1 null genotypes, respectively, and a 6.6-fold (95% Cl: 2.4-7.9) increased risk associated with the combined null genotype presents preliminary evidence that the inherited absence of this carcinogen detoxification pathway may be an important determinant of AML.pt
dc.relation.ispartofEuropean Journal Of Haematologypt_BR
dc.relation.ispartofabbreviationEur. J. Haematol.pt_BR
dc.publisher.cityCopenhagenpt_BR
dc.publisher.countryDinamarcapt_BR
dc.publisherMunksgaard Int Publ Ltdpt_BR
dc.date.issued2001pt_BR
dc.date.monthofcirculationJUNpt_BR
dc.identifier.citationEuropean Journal Of Haematology. Munksgaard Int Publ Ltd, v. 66, n. 6, n. 383, n. 388, 2001.pt_BR
dc.language.isoenpt_BR
dc.description.volume66pt_BR
dc.description.issuenumber6pt_BR
dc.description.firstpage383pt_BR
dc.description.lastpage388pt_BR
dc.rightsfechadopt_BR
dc.sourceWeb of Sciencept_BR
dc.identifier.issn0902-4441pt_BR
dc.identifier.wosidWOS:000170196700004pt_BR
dc.identifier.doi10.1034/j.1600-0609.2001.066006383.xpt_BR
dc.date.available2014-11-19T06:40:20Z
dc.date.available2015-11-26T17:03:22Z-
dc.date.accessioned2014-11-19T06:40:20Z
dc.date.accessioned2015-11-26T17:03:22Z-
dc.description.provenanceMade available in DSpace on 2014-11-19T06:40:20Z (GMT). No. of bitstreams: 1 WOS000170196700004.pdf: 96059 bytes, checksum: 66de8fbdce953549a419fb9502095b6d (MD5) Previous issue date: 2001en
dc.description.provenanceMade available in DSpace on 2015-11-26T17:03:22Z (GMT). No. of bitstreams: 2 WOS000170196700004.pdf: 96059 bytes, checksum: 66de8fbdce953549a419fb9502095b6d (MD5) WOS000170196700004.pdf.txt: 27936 bytes, checksum: 817be218e9008064dde63eb2d31cde78 (MD5) Previous issue date: 2001en
dc.identifier.urihttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/60033pt_BR
dc.identifier.urihttp://www.repositorio.unicamp.br/handle/REPOSIP/60033
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/60033-
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