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7. N-Acetylation phenotype and genotype and risk of bladder cancer in benzidine-exposed workers

Author

Hayes, Richard B., Bi, Wenfang, Rothman, Nathaniel, Broly, Franck, Caporaso, Neil, Feng, Peiwen, You, Xiejun, Yin, Songnian, Woosley, Raymond L., Meyer, Urs A., Hayes, Richard B., Bi, Wenfang, Rothman, Nathaniel, Broly, Franck, Caporaso, Neil, Feng, Peiwen, You, Xiejun, Yin, Songnian, Woosley, Raymond L., and Meyer, Urs A.

Abstract

Several studies in subjects occupationally exposed to arylamine carcinogens have shown increased risks for bladder cancer associated with the slow acetylator phenotype. To follow up these reports, a case-control study of N-acetylation and bladder cancer risk was carried out among subjects occupationally exposed to benzidine, in benzidine dye production and use facilities in China. Thirty-eight bladder cancer cases and 43 controls from these factories were included for study of acetylation phenotype, by dapsone administration, and for polymorphisms in the NAT2 gene, by a polymerase chain reaction (PCR)-based test. In contrast to previous studies, no increase in bladder cancer risk was found for the slow N-acetylation phenotype (OR= 0.3; 95% CI = 0.1-1.3) or for slow N-acetylation-associated double mutations in NAT2 (OR = 0.5; 95% CI = 0.1-1.8). Examination of specific mutations and adjustment for age, weight, city and tobacco use did not alter the results. When examined by level of benzidine exposure in the cases, the bladder cancer risks associated with low (OR = 0.3, 95% CI = 0.0-2.2), medium (OR = 0.7, 95% CI = 0.1-4.5) and high (OR = 0.6, 95% CI = 0.1-3.5) exposure showed no interaction between genotype and benzidine exposure, within the range of exposures experienced by subjects in this study. This study, which is the first to incorporate phenotypic and genotypic analyses, provides evidence that the NAT2-related slow N-acetylation polymorphism is not associated with an increased risk of bladder cancer in workers exposed to benzidine, and may have a protective effect

Published
2017

11. N-Acetylation phenotype and genotype and risk of bladder cancer in benzidine-exposed workers

Author

Hayes, Richard B., Bi, Wenfang, Rothman, Nathaniel, Broly, Franck, Caporaso, Neil, Feng, Peiwen, You, Xiejun, Yin, Songnian, Woosley, Raymond L., Meyer, Urs A., Hayes, Richard B., Bi, Wenfang, Rothman, Nathaniel, Broly, Franck, Caporaso, Neil, Feng, Peiwen, You, Xiejun, Yin, Songnian, Woosley, Raymond L., and Meyer, Urs A.

Abstract

Several studies in subjects occupationally exposed to arylamine carcinogens have shown increased risks for bladder cancer associated with the slow acetylator phenotype. To follow up these reports, a case-control study of N-acetylation and bladder cancer risk was carried out among subjects occupationally exposed to benzidine, in benzidine dye production and use facilities in China. Thirty-eight bladder cancer cases and 43 controls from these factories were included for study of acetylation phenotype, by dapsone administration, and for polymorphisms in the NAT2 gene, by a polymerase chain reaction (PCR)-based test. In contrast to previous studies, no increase in bladder cancer risk was found for the slow N-acetylation phenotype (OR= 0.3; 95% CI = 0.1-1.3) or for slow N-acetylation-associated double mutations in NAT2 (OR = 0.5; 95% CI = 0.1-1.8). Examination of specific mutations and adjustment for age, weight, city and tobacco use did not alter the results. When examined by level of benzidine exposure in the cases, the bladder cancer risks associated with low (OR = 0.3, 95% CI = 0.0-2.2), medium (OR = 0.7, 95% CI = 0.1-4.5) and high (OR = 0.6, 95% CI = 0.1-3.5) exposure showed no interaction between genotype and benzidine exposure, within the range of exposures experienced by subjects in this study. This study, which is the first to incorporate phenotypic and genotypic analyses, provides evidence that the NAT2-related slow N-acetylation polymorphism is not associated with an increased risk of bladder cancer in workers exposed to benzidine, and may have a protective effect

12. Interaction of PGC7 and HP1BP3 Maintains Meg3-DMR Methylation by Regulating Chromatin Configuration.

Author

Liu Y, Hao W, Huang C, Feng P, Liu H, and Guo Z

Subjects
Animals, Mice, DNA Methyltransferase 3A metabolism, Humans, DNA (Cytosine-5-)-Methyltransferases metabolism, DNA (Cytosine-5-)-Methyltransferases genetics, Histones metabolism, Histones genetics, DNA Methylation, Genomic Imprinting, Chromatin metabolism, Chromatin genetics, RNA, Long Noncoding genetics, RNA, Long Noncoding metabolism
Abstract

Genomic imprinting is essential for mammalian development. PGC7, an important maternal factor, binds to dimethylated histone H3K9 (H3K9me2), maintaining DNA methylation in zygotes and stem cells. However, the underlying molecular mechanisms of PGC7-maintained genomic imprinting in stem cells are not clear. Our previous study has identified that PGC7 interacts with HP1BP3, a novel member of the histone H1 family. In this study, we found that PGC7 interacts with the central globular domain of HP1BP3 through its C-terminal tail and that HP1BP3 is responsible for the recruitment of PGC7 at the Meg3 differentially methylated region (DMR) in the Dlk1-Dio3 imprinted domain. HP1BP3 or PGC7 depletion decreases enrichment in the Meg3-DMR, leading to DNA hypermethylation in this region. Moreover, the cooperative binding of PGC7 and HP1BP3 can antagonize the enrichment of DNMT3A in the Meg3-DMR, and the depletion of HP1BP3 or PGC7 separately induces chromosome decondensation in this region. In summary, this is the first study demonstrating that PGC7 and HP1BP3 synergistically maintain the methylation status of the Meg3-DMR by enabling a chromatin configuration that interferes with the binding of the de novo DNA methyltransferase DNMT3A., (© 2024 Wiley Periodicals LLC.)

Published
2025
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