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Risks on N-acetyltransferase 2 and bladder cancer: a meta-analysis
Zongheng Zhu1, Jinshan Zhang2, Wei Jiang3
1Department of General Surgery, Huangshi Love & Health Hospital, Huangshi, People's Republic of China.
Background:
It is known that bladder cancer disease is closely related to aromatic amine compounds, which could cause cancer by regulating of N-acetylation and N-acetyltransferase 1 and 2 (NAT1 and NAT2). The NAT2 slowed acetylation and would increase the risk of bladder cancer, with tobacco smoke being regarded as a risk factor for this increased risk. However, the relationship between NAT2 slow acetylation and bladder cancer is still debatable at present. This study aims to explore preliminarily correlation of NAT2 slow acetylation and the risk of bladder cancer.
Methods:
The articles were searched from PubMed, Cochran, McGrane English databases, CBM, CNKI, and other databases. The extraction of bladder cancer patients and a control group related with the NAT2 gene were detected by the state, and the referenced articles and publications were also used for data retrieval. Using a random effects model, the model assumes that the studies included in the analysis cases belong to the overall population in the study of random sampling, and considering the variables within and between studies. Data were analyzed using STATA Version 6.0 software, using the META module. According to the inclusion and exclusion criteria of the literature study, 20 independent studies are included in this meta-analysis.
Results:
The results showed that the individual differences of bladder cancer susceptibility might be part of the metabolism of carcinogens. Slow acetylation status of bladder cancer associated with the pooled odds ratio was 1.31 (95% confidence interval: 1.11-1.55).
Conclusion:
The status of NAT2 slow N-acetylation is associated with bladder cancer risks, and may increase the risk of bladder cancer.
Insights
Individuals with NAT2 slow N-acetylation may have an increased risk of bladder cancer. This meta-analysis suggests a correlation between slow NAT2 acetylation status and bladder cancer susceptibility.
Area of Science:
- Oncology
- Genetics
- Pharmacogenomics
Background:
- Bladder cancer is linked to aromatic amine compounds.
- N-acetyltransferase 1 and 2 (NAT1 and NAT2) regulate N-acetylation, influencing cancer risk.
- NAT2 slow acetylation is a debated risk factor for bladder cancer, potentially exacerbated by tobacco smoke.
Purpose of the Study:
- To investigate the correlation between NAT2 slow N-acetylation and the risk of bladder cancer.
- To provide preliminary evidence on the role of NAT2 acetylation status in bladder cancer development.
Main Methods:
- A meta-analysis was conducted, including 20 independent studies.
- Data were retrieved from multiple databases (PubMed, Cochran, McGrane, CBM, CNKI).
- A random effects model was used for data analysis with STATA software.
Main Results:
- Slow acetylation status of NAT2 was associated with bladder cancer.
- The pooled odds ratio for bladder cancer in individuals with slow NAT2 acetylation was 1.31 (95% CI: 1.11-1.55).
- Individual differences in carcinogen metabolism may contribute to bladder cancer susceptibility.
Conclusions:
- NAT2 slow N-acetylation status is associated with an increased risk of bladder cancer.
- This finding supports the role of genetic variations in NAT2 in bladder cancer etiology.
