Evidence map›Paper›PMID 17434923›Full record

ArticleCarcinogenesis2007

Functional characterization of single-nucleotide polymorphisms and haplotypes of human N-acetyltransferase 2.

Yu Zang, Mark A Doll, Shuang Zhao, J Christopher States, David W Hein

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
3.6field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 110 citations in OpenAlex.

  1. Pharmacogenetic association betweenBioscience reports · 2019
    Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Pharmacogenomic heterogeneity ofAnnals of medicine · 2025
    Observational
  6. Associations of Cruciferous Vegetable Intake with Breast Cancer Survival in a Diverse Population in the Pathways Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2025
    Article
  7. Article
  8. Precision Medicine Strategies to Improve Isoniazid Therapy in Patients with Tuberculosis.European journal of drug metabolism and pharmacokinetics · 2024
    Review
  9. Article
  10. Article
  11. Human N-acetyltransferase 2 (Frontiers in pharmacology · 2023
    Article
  12. Article
  13. Article
  14. HumanFrontiers in pharmacology · 2022
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Yu ZangDepartment of Pharmacology and Toxicology, James Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY 40292, USA.
Mark A Doll
Shuang Zhao
J Christopher States
David W Hein
University of Louisville · US

Funding

PHARMACOGENETICS OF DRUG &CARCINOGEN METABOLISMR01CA034627 · NCI · UNIVERSITY OF NORTH DAKOTA · PI HEIN, DAVID W · 1985 to 2009
$3.1M
NCI NIH HHS CA-34627NCI NIH HHS R01 CA034627
6 · The paper itself

Abstract

Human N-acetyltransferase 2 (NAT2) is polymorphic in humans and may associate with cancer risk by modifying individual susceptibility to cancers from carcinogen exposure. Since molecular epidemiological studies investigating these associations usually include determining NAT2 single-nucleotide polymorphisms (SNPs), haplotypes or genotypes, their conclusions can be compromised by the uncertainty of genotype-phenotype relationships. We characterized NAT2 SNPs and haplotypes by cloning and expressing recombinant NAT2 allozymes in mammalian cells. The reference and variant recombinant NAT2 allozymes were characterized for arylamine N-acetylation and O-acetylation of N-hydroxy-arylamines. SNPs and haplotypes that conferred reduced enzymatic activity did so by reducing NAT2 protein without changing NAT2 mRNA levels. Among SNPs that reduced catalytic activity, G191A (R64Q), G590A (R197Q) and G857A (G286E) reduced protein half-life but T341C (I114T), G499A (E167K) and A411T (L137F) did not. G857A (G286E) and the major haplotype possessing this SNP (NAT2 7B) altered the affinity to both substrate and cofactor acetyl coenzyme A, resulting in reduced catalytic activity toward some substrates but not others. Our results suggest that coding region SNPs confer slow acetylator phenotype by multiple mechanisms that also may vary with arylamine exposures.

Indexed as

HaplotypesPolymorphism, Single NucleotideAcetylationAnimalsArylamine N-AcetyltransferaseChlorocebus aethiopsCOS CellsHumansPhenotypeSulfamethazineArylamine N-AcetyltransferaseNAT2 protein, humanSulfamethazine

Identifiers

PMID17434923
PMCPMC2085371
OpenAlexW2102433970

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.