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Báo cáo y học: " Genetic polymorphisms in glutathione S-transferase (GST) superfamily and risk of arsenic-induced urothelial carcinoma in residents of southwestern Taiwan"

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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Genetic polymorphisms in glutathione S-transferase (GST) superfamily and risk of arsenic-induced urothelial carcinoma in residents of southwestern Taiwan | Hsu et al. Journal of Biomedical Science 2011 18 51 http www.jbiomedsci.eom content 18 1 51 tì.NSC The cost of publication in Journal of Biomedical Science Is borne by the National Science Council Taiwan JOURNAL OF BIOMEDICAL SCIENCE RESEARCH Open Access Genetic polymorphisms in glutathione S-transferase GST superfamily and risk of arsenic-induced urothelial carcinoma in residents of southwestern Taiwan 1 1 1 1 1 2.3 4 Ling-I Hsu Wu-Ping Chen Tse-Yen Yang Yu-Hsin Chen Wann-Cheng Lo Yuan-Hung Wang Ya-Tang Liao Yu-Mei Hsueh2 Hung-Yi Chiou2 Meei-Maan Wu1 and Chien-Jen Chen1 Abstract Background Arsenic exposure is an important public health issue worldwide. Dose-response relationship between arsenic exposure and risk of urothelial carcinoma UC is consistently observed. Inorganic arsenic is methylated to form the metabolites monomethylarsonic acid and dimethylarsinic acid while ingested. Variations in capacity of xenobiotic detoxification and arsenic methylation might explain individual variation in susceptibility to arsenic-induced cancers. Methods To estimate individual susceptibility to arsenic-induced UC 764 DNA specimens from our long-term follow-up cohort in Southwestern Taiwan were used and the genetic polymorphisms in GSTM1 GSTT1 GSTP1 and arsenic methylation enzymes including GSTO1 and GSTO2 were genotyped. Results The GSTT1 null was marginally associated with increased urothelial carcinoma UC risk HR 1.91 95 CI 1.00-3.65 while the association was not observed for other GSTs. Among the subjects with cumulative arsenic exposure CAE 20 mg L year the GSTT1 null genotype conferred a significantly increased cancer risk RR 3.25 95 CI 1.20-8.80 . The gene-environment interaction between the GSTT1 and high arsenic exposure with respect to cancer risk was statistically significant multiplicative model p 0.0151 and etiologic fraction was as high as 0.86 95 CI 0.51-1.22 . The genetic effects of GSTO1 GSTO2 were largely confined to high arsenic level CAE 20 . Diplotype .

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