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Effects of glutathione S-transferase (GST) M1 and GSTT1 genotypes on urothelial cancer risk

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dc.contributor.authorKatoh, T.-
dc.contributor.authorInatomi, H.-
dc.contributor.authorKim, H.-
dc.contributor.authorYang, M.-
dc.contributor.authorMatsumoto, T.-
dc.contributor.authorKawamoto, T.-
dc.date.accessioned2022-04-19T13:21:58Z-
dc.date.available2022-04-19T13:21:58Z-
dc.date.issued1998-10-
dc.identifier.issn0304-3835-
dc.identifier.issn1872-7980-
dc.identifier.urihttps://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/150228-
dc.description.abstractThe M1 member of the mu class of the glutathione S-transferase (GSTM1) gene is present in about 50% of individuals. GSTT1, a member of the theta class, which has been recently shown to be polymorphic, is expressed in 35-90% of individuals. In this study, 145 Japanese patients with urothelial transitional cell carcinoma and 145 healthy controls, frequency-matched for age and gender, were compared for frequencies of GSTM1 and GSTT1 genotypes. The urothelial cancer risk increased due to the GSTM1 null genotype (odds ratio (OR) 1.71, 95% confidence interval (CI) 1.05-2.79). On the other hand, the OR tended to decrease due to the GSTT1 null genotype, although not significantly. Among individuals of the GSTM1 null genotype, those of the GSTT1-positive genotype had a two-fold risk (OR 2.62, 95% CI 1.36-5.05) compared with the GSTT1 null genotype (OR 1.25, 95% CI 0.62-2.51). A significant interaction between the GSTM1 genotype and smoking status was found; the GSTM1 null genotype was associated with an increased risk of urothelial cancer among smokers (OR 1.98, 95%CI 1.10-3.57). Copyright (C) 1998 Elsevier Science Ireland Ltd.-
dc.format.extent6-
dc.language영어-
dc.language.isoENG-
dc.publisherElsevier BV-
dc.titleEffects of glutathione S-transferase (GST) M1 and GSTT1 genotypes on urothelial cancer risk-
dc.typeArticle-
dc.publisher.location아일랜드-
dc.identifier.doi10.1016/S0304-3835(98)00183-9-
dc.identifier.scopusid2-s2.0-0032561158-
dc.identifier.wosid000077278500021-
dc.identifier.bibliographicCitationCancer Letters, v.132, no.1-2, pp 147 - 152-
dc.citation.titleCancer Letters-
dc.citation.volume132-
dc.citation.number1-2-
dc.citation.startPage147-
dc.citation.endPage152-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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