ArticleInternational journal of clinical and experimental medicine2015
NAT1 polymorphisms and cancer risk: a systematic review and meta-analysis.
Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Association ofMedicina (Kaunas, Lithuania) · 2021Pooled it
- Regulation of NAT1 activity in modern humans by a novel phosphorylation site.Science advances · 2026Article
- Identification and characterization of potent, selective, and efficacious inhibitors of human arylamine N-acetyltransferase 1.Archives of toxicology · 2022Article
- 560G>A (rs4986782) (R187Q) Single Nucleotide Polymorphism in Arylamine N-Acetyltransferase 1 Increases Affinity for the Aromatic Amine Carcinogens 4-Aminobiphenyl and N-Hydroxy-4-Aminobiphenyl: Implications for Cancer Risk Assessment.Frontiers in pharmacology · 2022Article
- Gene polymorphisms and risk of head and neck squamous cell carcinoma: a systematic review.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2022Review
- Functional expression of human arylamine N-acetyltransferase NAT1*10 and NAT1*11 alleles: a mini review.Pharmacogenetics and genomics · 2018Review
- High N-Acetyltransferase 1 Expression Is Associated with Estrogen Receptor Expression in Breast Tumors, but Is not Under Direct Regulation by Estradiol, 5The Journal of pharmacology and experimental therapeutics · 2018Article
- Predicting radiotherapy response for patients with soft tissue sarcoma by developing a molecular signature.Oncology reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo investigate the association between the N-acetyltransferase 1 (NAT1) slow and rapid acetylation phenotypes with cancer risk based on a meta-analysis.
methodsPreviously published case-control studies were retrieved from PubMed, Embase, and Web of Science. Odds ratios (ORs) with 95% confidence intervals (CIs) were determined to assess the relationship between NAT1 polymorphisms and cancer risk.
resultsA total of 73 studies (24874 cases and 30226 controls) were included in this meta-analysis. No significant association was identified between NAT1 polymorphisms (slow acetylation versus rapid acetylation genotypes: OR = 0.978, 95% CI = 0.927-1.030, P < 0.001 for heterogeneity, I(2) = 45.5%) and cancer risk, whereas a significantly reduced risk of pancreatic cancer was identified in individuals with NAT1 slow acetylation genotype (OR = 0.856, 95% CI = 0.733-0.999, P =0.509 for heterogeneity, I(2) = 0). When the NAT1 slow acetylation genotype was analysed on the basis of stratified analyses of ethnicity, a significantly reduced risk of head and neck cancers was found among Asian (OR=0.281, 95% CI = 0.127-0.622). When the NAT1 slow acetylation genotype was analysed on the basis of stratified analyses of source of control, only significantly reduced risks of colorectal cancer (OR = 0.882, 95% CI = 0.798- 0.974, P = 0.212 for heterogeneity, I(2) = 22.9) and pancreatic cancer (OR=0.856, 95% CI = 0.733-0.999, P = 0.509 for heterogeneity, I(2) = 0) were found among hospital-based studies.
conclusionsNo significant association between the NAT1 polymorphisms and the risk of cancer was found except for pancreatic cancer.
Indexed as
Identifiers
26309576PMC4537954W1167932164What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.