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Effect of genetic polymorphisms of metabolic enzymes on benzidine-induced bladder cancer in Chinese workers: A nested case-control study.

机译：代谢酶基因多态性对联苯胺诱发的中国工人膀胱癌的影响：一项嵌套病例对照研究。

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摘要

The slow NAT2 N-acetylation genotype inhibits detoxification of a range of monoarylamines and has been associated with increased risk for bladder cancer in cigarette smokers and workers in arylamine dye production. The diarylamine, benzidine, is also a strong bladder carcinogen; however, NAT2 N-acetylation is not key to its detoxification. The purpose of this study was to expand on previous studies that evaluated the impact of NAT2 and GSTM1 polymorphisms on bladder cancer in male subjects exposed only to benzidine. This study also explored possible associations between mutant forms of metabolic enzymes ( NAT1, GSTT1, GSTP1, and UGT1A1) and bladder cancer risk.; This study included 30 cases and 67 controls exposed occupationally to benzidine in China. In addition, pooled analyses were conducted for NAT2 and GSTM1, incorporating a previous case-control study from the same cohort, for a final study size of 68 cases and 107 controls. NAT2 enzymatic activity was characterized by measuring urinary caffeine metabolite ratios as phenotypic markers. PCR-based methods were used to identify genotypes for the following genes: NAT2, NAT1, GSTM1, GSTT1, GSTP1, and UGT1A1.; Using the pooled data adjusted for cumulative benzidine exposure and smoking, a protective association was observed for the slow NAT2 genotype (bladder cancer OR = 0.3, 95% CI 0.11–0.99). NAT2 phenotype results were consistent with NAT2 genotype data. The risk of bladder cancer for the GSTM1-null genotype was 1.1 (95% CI 0.58–2.26).; Individuals carrying the rapid NAT1 allele showed a higher but not statistically significant risk of bladder cancer (OR = 2.3, 95% CI 0.8–7.1). The GSTT1 null polymorphism showed no association with bladder cancer risk; frequencies of the rare alleles for CYP1A1, GSTP1 and UGT1A1 were too low for analysis.; Study findings are consistent with other studies conducted in populations exposed only to benzidine. The data actually suggest decreased risk for benzidine-induced bladder cancer among NAT2 slow acetylators, although the mechanism for risk is not clearly understood. These results indicate the existence of key differences in the metabolism of mono- and diarylamines that combine with genotype to affect the individual susceptibility to bladder cancer.
机译：缓慢的NAT2 N -乙酰化基因型抑制一系列单芳基胺的解毒作用，并与吸烟者和芳基胺染料生产工人的膀胱癌风险增加相关。二芳基胺，联苯胺，也是一种很强的膀胱致癌物。然而，NAT2 N -乙酰化并不是其解毒的关键。这项研究的目的是扩展以前的研究，该研究评估了 NAT2 和 GSTM1 多态性对仅接触联苯胺的男性受试者膀胱癌的影响。这项研究还探讨了代谢酶突变形式（ NAT1，GSTT1，GSTP1 和 UGT1A1 ）与膀胱癌风险之间的可能联系。这项研究包括30例中国职业性接触联苯胺的病例和67名对照。此外，对 NAT2 和 GSTM1 进行了汇总分析，并纳入了同一队列中以前的病例对照研究，最终研究规模为68例和107例对照。 NAT2酶活性的特征是通过测量尿咖啡因代谢物的比例作为表型标记。使用PCR方法鉴定以下基因的基因型： NAT2，NAT1，GSTM1，GSTT1，GSTP1 和 UGT1A1 。使用针对累积的联苯胺暴露和吸烟进行调整的汇总数据，观察到缓慢的 NAT2 基因型（膀胱癌OR = 0.3，95％CI 0.11-0.99）的保护性关联。 NAT2表型结果与 NAT2 基因型数据一致。 GSTM1 -无效基因型的膀胱癌风险为1.1（95％CI 0.58–2.26）。携带快速 NAT1 等位基因的个体显示出较高的膀胱癌风险，但无统计学意义（OR = 2.3，95％CI 0.8-7.1）。 GSTT1 无效多态性与膀胱癌风险无关。 CYP1A1，GSTP1 和 UGT1A1 的罕见等位基因频率太低，无法进行分析。研究结果与仅接触联苯胺的人群中进行的其他研究一致。数据实际上暗示了NAT2慢速乙酰化剂中联苯胺诱发的膀胱癌的风险降低，尽管尚不清楚该风险的机制。这些结果表明，单芳基胺和二芳基胺的代谢中存在关键差异，这些差异与基因型相结合会影响个体对膀胱癌的易感性。

著录项

  • 作者

    Carreon Valencia, Tania.;

  • 作者单位

    University of Cincinnati.;

  • 授予单位 University of Cincinnati.;
  • 学科 Health Sciences Occupational Health and Safety.; Biology Molecular.
  • 学位 Ph.D.
  • 年度 2001
  • 页码 295 p.
  • 总页数 295
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 职业性疾病预防;分子遗传学;
  • 关键词

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