Evidence map›Paper›PMID 16550165›Full record

ReviewOncogene2006

N-acetyltransferase 2 genetic polymorphism: effects of carcinogen and haplotype on urinary bladder cancer risk.

D W Hein

Open access · bronzeAbstract readReview
In one paragraph

Review in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
9.7field-weighted citation impact, top 2% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 182 citations in OpenAlex.

  1. Pooled it
  2. Human N-acetyltransferase 2 (Frontiers in pharmacology · 2023
    Article
  3. Article
  4. Article
  5. Review
  6. Acetyl coenzyme A kinetic studies onFrontiers in pharmacology · 2022
    Article
  7. Review
  8. Case Study 10: A Case to Investigate Acetyl Transferase Kinetics.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Arylamine N-acetyltransferases: a structural perspective.British journal of pharmacology · 2013
    Review

7 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

D W HeinDepartment of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY 40292, USA. d.hein@louisville.edu
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 R01 CA034627NCI NIH HHS R01-CA34627
6 · The paper itself

Abstract

A role for the N-acetyltransferase 2 (NAT2) genetic polymorphism in cancer risk has been the subject of numerous studies. Although comprehensive reviews of the NAT2 acetylation polymorphism have been published elsewhere, the objective of this paper is to briefly highlight some important features of the NAT2 acetylation polymorphism that are not universally accepted to better understand the role of NAT2 polymorphism in carcinogenic risk assessment. NAT2 slow acetylator phenotype(s) infer a consistent and robust increase in urinary bladder cancer risk following exposures to aromatic amine carcinogens. However, identification of specific carcinogens is important as the effect of NAT2 polymorphism on urinary bladder cancer differs dramatically between monoarylamines and diarylamines. Misclassifications of carcinogen exposure and NAT2 genotype/phenotype confound evidence for a real biological effect. Functional understanding of the effects of NAT2 genetic polymorphisms on metabolism and genotoxicity, tissue-specific expression and the elucidation of the molecular mechanisms responsible are critical for the interpretation of previous and future human molecular epidemiology investigations into the role of NAT2 polymorphism on cancer risk. Although associations have been reported for various cancers, this paper focuses on urinary bladder cancer, a cancer in which a role for NAT2 polymorphism was first proposed and for which evidence is accumulating that the effect is biologically significant with important public health implications.

Indexed as

Polymorphism, GeneticAcetylationAminesArylamine N-AcetyltransferaseCarcinogensGenotypeHaplotypesHumansMolecular EpidemiologyPhenotypeRisk AssessmentRisk FactorsUrinary Bladder NeoplasmsAminesArylamine N-AcetyltransferaseCarcinogensNAT2 protein, human

Identifiers

PMID16550165
PMCPMC1434721
OpenAlexW1979047461

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.