Corpus ID: 7440844

Current smoking, occupation, N-acetyltransferase-2 and bladder cancer: a pooled analysis of genotype-based studies.

@article{Vineis2001CurrentSO,
  title={Current smoking, occupation, N-acetyltransferase-2 and bladder cancer: a pooled analysis of genotype-based studies.},
  author={P. Vineis and D. Marinelli and H. Autrup and J. Brockmoller and I. Cascorbi and A. Daly and K. Golka and H. Okkels and A. Risch and N. Rothman and E. Sim and E. Taioli},
  journal={Cancer epidemiology, biomarkers \& prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology},
  year={2001},
  volume={10 12},
  pages={
          1249-52
        }
}
  • P. Vineis, D. Marinelli, +9 authors E. Taioli
  • Published 2001
  • Medicine
  • Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
The aim of this study was to investigate the association of NAT2 gene polymorphism with bladder cancer using the data derived from the International Project on Genetic Susceptibility to Environmental Carcinogens. Four case control studies conducted in four European countries, plus two case series, one from England and one from Germany, for a total of 1530 cases and 731 controls (all Caucasian) were included. The interaction between NAT2 and bladder cancer considering smoking habits and… Expand
N-acetyltransferase 2 Phenotype, Occupation, and Bladder Cancer Risk: Results from the EPIC Cohort
TLDR
These findings confirm established or suspected occupational risk factors but not the anticipated role of NAT2 slow acetylation in bladder cancer. Expand
Cigarette Smoking, N-Acetyltransferase 2 Genotypes, and Breast Cancer Risk: Pooled Analysis and Meta-analysis
TLDR
The results show that cigarette smoking is associated with an increase in breast cancer risk among women with NAT2 slow acetylation genotypes, and because slow NAT2 genotypes are present in 50% to 60% of Caucasian populations, smoking is likely to play an important role in Breast cancer etiology. Expand
NAT 2 slow acetylation , GSTM 1 null genotype , and risk of bladder cancer : results from the Spanish Bladder Cancer Study and meta-analyses
Introduction The inability to replicate results on many associations between common genetic polymorphisms and complex diseases has raised scepticism in this area of research. One of the fewExpand
NAT2 fast acetylator genotype is associated with an increased risk of lung cancer among never-smoking women in Taiwan.
TLDR
Results suggested never-smoking females with NAT2 fast acetylator were more prone to lung cancer and reflected the possibility that exposure to heterocyclic amines may contribute to the female lung cancer development in Taiwan. Expand
Effects of N-acetyl transferase 1 and 2 polymorphisms on bladder cancer risk in Caucasians.
TLDR
The data suggest that having a NAT2 slow acetylator genotype is a significant risk factor for BC, particularly in smokers and older individuals, and a joint effect between NAT2slow acetylators and heavy smokers was observed. Expand
Effect of NAT2 gene polymorphism on bladder cancer risk in Slovak population
TLDR
Findings are consistent with previous literature suggesting that individual susceptibility to bladder cancer may be modulated by NAT2 polymorphisms, particularly in interaction with relevant environmental exposures such as smoking. Expand
NAT2 slow acetylation, GSTM1 null genotype, and risk of bladder cancer: results from the Spanish Bladder Cancer Study and meta-analyses
TLDR
The GSTM1 null genotypes increases the overall risk of bladder cancer, and the NAT2 slow-acetylator genotype increases risk particularly among cigarette smokers, providing compelling evidence for the role of common polymorphisms in the aetiology of cancer. Expand
Meat intake and bladder cancer in a prospective study: a role for heterocyclic aromatic amines?
TLDR
The hypothesis that among subjects with the rapid NAT2 acetylation genotype higher levels of HAAs exposure are a bladder cancer risk factor is supported, as well as the possible long-term adverse effects of diets with high meat intake. Expand
Genetic determinants in the metabolism of bladder carcinogens in relation to risk of bladder cancer.
TLDR
Individual null/low-activity genotypes of GSTM1, GSTT1 and GSTP1 were associated with a 19-48% increase in odds ratio (OR) of bladder cancer, and the effect of NAT2 slow acetylation was even stronger in the presence of two or more null/ low-activity GST genotypes. Expand
Evidence for an intensity-dependent interaction of NAT2 acetylation genotype and cigarette smoking in the Spanish Bladder Cancer Study.
TLDR
A comprehensive three-parameter linear-exponential model for the excess odds ratio for smoking to include effects of NAT2 status reveals an enhanced effect for smoking intensity and bladder cancer in NAT2 slow acetylators which increases with intensity. Expand
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References

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TLDR
The published evidence suggests that NAT2 slow acetylator phenotype or genotype may be associated with a small increase in bladder cancer risk, but the current evidence is not sufficient to conclude that there is a real increase in risk. Expand
Slow N-acetylation genotype is a susceptibility factor in occupational and smoking related bladder cancer.
TLDR
Slow NAT genotype is therefore a contributory risk factor in bladder carcinogenesis which acts through influencing individual response to environmental carcinogens. Expand
Cigarette smoking, N-acetyltransferase 2 acetylation status, and bladder cancer risk: a case-series meta-analysis of a gene-environment interaction.
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A meta-analysis using data from 16 bladder cancer studies conducted in the general population and using a case-series design to assess multiplicative gene-environment interaction suggests that the relationship of smoking and bladder cancer is stronger among slow acetylators than among rapid acetylator. Expand
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TLDR
According to the data, slow acetylators with 341C/341C and341C/857A genotypes carry a substantially higher odds ratio for bladder carcinogenesis and homozygotes are likely to have a higher risk for more aggressive disease. Expand
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TLDR
In most populations studied to date, NAT2 slow acetylation status is associated with a modest increase in bladder cancer risk, and statistical tests indicated that pooling of all studies, or of studies conducted in Caucasian populations, hid potentially important heterogeneity in the individual study results. Expand
N‐acetyl transferase‐2 and bladder cancer risk: A meta‐analysis
TLDR
The results suggest that NAT2 slow acetylator status is associated with a modest increase in risk of bladder cancer, and greater attention should be paid to the design of study. Expand
White blood cell DNA adducts, smoking, and NAT2 and GSTM1 genotypes in bladder cancer: a case-control study.
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  • Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
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TLDR
Analyses of genetic combinations of NAT1/NAT2 as potential risk factors for bladder cancer seem to indicate that the normal NAT2/fast NAT2 genotype may be a protective genotype compared with the other genotype combinations. Expand
The role of N-acetylation polymorphisms in smoking-associated bladder cancer: evidence of a gene-gene-exposure three-way interaction.
TLDR
Interestingly, although NAT2 genotype did not influence risk either alone or in combination with smoking exposure, there was evidence of a statistically significant gene-gene-environment three-way interaction, such that bladder cancer risk depends on both NAT1 genotype and smoking exposure. Expand
N-Acetyltransferase 2 (NAT2) and Glutathione S-Transferase µ (GSTM1) in Bladder-cancer Patients in a Highly Industrialized Area.
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  • Medicine
  • International journal of occupational and environmental health
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TLDR
The results are consistent with the view that a slow-acetylator status and lack of the GSTM1 gene are individual risk factors for bladder cancer in persons occupationally exposed to aromatic amines and PAHs. Expand
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