ArticleGenetics and molecular biology2012
Polymorphisms of arylamine N-acetyltransferase2 and risk of lung and colorectal cancer.
Article in Genetics and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 3 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Pooled it
- Association Between NAT2 Polymorphism and Lung Cancer Risk: A Systematic Review and Meta-Analysis.Frontiers in oncology · 2021Pooled it
- Pooled it
- Investigating the genetic landscape of cancer in Jordan: a step toward personalized care.European journal of medical research · 2025Review
- Variation in 100 relevant pharmacogenes among emiratis with insights from understudied populations.Scientific reports · 2020Article
- NAT2 gene diversity and its evolutionary trajectory in the Americas.The pharmacogenomics journal · 2016Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The arylamine N-acetyltransferase 2 (NAT2) enzymes detoxify a wide range of naturally occurring xenobiotics including carcinogens and drugs. Point mutations in the NAT2 gene result in the variant alleles M1 (NAT2 *5A), M2 (NAT2*6A), M3 (NAT2*7) and M4 (NAT2 *14A) from the wild-type WT (NAT2 *4) allele. The current study was aimed at screening genetic polymorphisms of NAT2 gene in 49 lung cancer patients, 54 colorectal cancer patients and 99 cancer-free controls, using PCR-RFLP. There were significant differences in allele frequencies between lung cancer patients and controls in the WT, M2 and M3 alleles (p < 0.05). However, only M2 and M3 allele frequencies were different between colorectal cancer patients and controls (p < 0.05). There was a marginal significant difference in the distribution of rapid and slow acetylator genotypes between lung cancer patients and controls (p = 0.06 and p = 0.05, respectively), but not between colorectal cancer patients and controls (p = 1.0 and p = 0.95, respectively). Risk of lung cancer development was found to be lower in slow acetylators [odds ratio (OR): 0.51, 95% confidence interval (95% CI): 0.25, 1.02, p-value = 0.07]. No effect was observed in case of colorectal cancer. Our results showed that NAT2 genotypes and phenotypes might be involved in lung cancer but not colorectal cancer susceptibility in Jordan.
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