Glutathione sulfur transferase M1 and T1 genotypes in chronic lymphoblastic leukemia

dc.contributor.authorTsabouri, S.en
dc.contributor.authorGeorgiou, I.en
dc.contributor.authorKatsaraki, A.en
dc.contributor.authorBourantas, K. L.en
dc.date.accessioned2015-11-24T19:14:39Z
dc.date.available2015-11-24T19:14:39Z
dc.identifier.issn1466-4860-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/21360
dc.rightsDefault Licence-
dc.subjectAgeden
dc.subjectAged, 80 and overen
dc.subjectDisease Progressionen
dc.subjectFemaleen
dc.subjectGene Deletionen
dc.subjectGene Frequencyen
dc.subjectGenetic Predisposition to Diseaseen
dc.subjectGenotypeen
dc.subjectGlutathione Transferase/*geneticsen
dc.subjectGreeceen
dc.subjectHomozygoteen
dc.subjectHumansen
dc.subjectLeukemia, Lymphocytic, Chronic, B-Cell/diagnosis/*geneticsen
dc.subjectMaleen
dc.subjectMiddle Ageden
dc.subjectOdds Ratioen
dc.subjectRisk Factorsen
dc.titleGlutathione sulfur transferase M1 and T1 genotypes in chronic lymphoblastic leukemiaen
heal.abstractGlutathione sulfur transferases (GSTs) is a group of enzymes involved in the detoxification process of carcinogens and other substances. The genes encoding isoenzymes M1 and T1 are polymorphic in humans and the phenotypic absence of enzyme activity (null genotype) may have an effect on the risk of chronic lymphoblastic leukemia (CLL). Our purpose was to examine whether the GSTM1 and GSTT1 homozygous null genotypes altered the risk of CLL. DNA was extracted from the peripheral blood of 27 patients with CLL and 147 cancer-free controls; both groups originated from a defined population (residents of the Ioannina region, northwestern Greece) and were similar with regard to mean age, race and sex; GSTM1 and GSTT1 were simultaneously analyzed by a multiplex polymerase chain reaction (PCR) method and Fisher's exact test was used for comparisons between the two groups. A significantly increased incidence of the GSTM1 null genotype was found in the group of patients compared to the controls (74.07 versus 34.69%, P = 0.0002). Additionally, the incidence of the GSTT1 null genotype was comparable in patients and controls (25.92 versus 10.20%, P = 0.05). The frequency of the combined GSTM1 null/T1 null genotype was significantly different between patients and controls (14.81 versus 2.04%, P = 0.012). However, there was no relationship between the advanced stage of the disease and the GSTs status. Individuals with the GSTM1 and GSTT1 null genotypes may have enhanced susceptibility to CLL.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.primary10.1038/sj.thj.6200555-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/15570292-
heal.journalNameHematol Jen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2004-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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