Evidence map›Paper›PMID 28092945›Full record

ArticleChemical research in toxicology2017

Nicotine Metabolism and Smoking: Ethnic Differences in the Role of P450 2A6.

Sharon E Murphy

Open access · greenAbstract read
In one paragraph

Article in Chemical research in toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 64 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
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  7. Impact of Genetic Variants in the Nicotine Metabolism Pathway on Nicotine Metabolite Levels in Smokers.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2023
    Article
  8. Contribution of Genetic Polymorphisms in Human Health.International journal of environmental research and public health · 2023
    Review
  9. CYP2C19 Plays a Major Role in the HepaticDrug metabolism and disposition: the biological fate of chemicals · 2023
    Article
  10. Article
  11. Urinary Nicotine Metabolites and Self-Reported Tobacco Use Among Adults in the Population Assessment of Tobacco and Health (PATH) Study, 2013-2014.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2022
    Article
  12. Article
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  15. Review
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  19. Applying Tobacco, Environmental, and Dietary-Related Biomarkers to Understand Cancer Etiology and Evaluate Prevention Strategies.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020
    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

1 author at 1 institution in 1 country.

Sharon E MurphyDepartment of Biochemistry, Molecular Biology, and Biophysics and Masonic Cancer Center, University of Minnesota , Minneapolis, Minnesota 55455, United States.ORCID 0000-0001-5391-8104
University of Minnesota · US

Funding

Untargeted Adductomics to Characterize Ethnic Differences in the Exposome of SmokersP01CA138338 · NCI · UNIVERSITY OF MINNESOTA · PI Daniel O Stram · 2010 to 2026
$33.4M
NCI NIH HHS P01 CA138338
6 · The paper itself

Abstract

Nicotine is the primary addictive agent in tobacco, and P450 2A6 (gene name: CYP2A6) is the primary catalyst of nicotine metabolism. It was proposed more than 20 years ago that individuals who metabolize nicotine poorly would smoke less, either fewer cigarettes per day or less intensely per cigarette, compared to smokers who metabolize nicotine more efficiently. These poor metabolizers would then be less likely to develop lung cancer due to their lower exposure to the many carcinogens delivered with nicotine in each puff of smoke. Numerous studies have reported that smokers who carry reduced activity or null CYP2A6 alleles do smoke less. Yet only in Asian populations, both Japanese and Chinese, which have a high prevalence of genetic variants, has a link between CYP2A6, smoking dose, and lung cancer been established. In other ethnic groups, it has been challenging to confirm a direct link between P450 2A6-mediated nicotine metabolism and the risk of lung cancer. This challenge is due in part to the difficulty in accurately quantifying smoking dose and accurately predicting or measuring P450 2A6-mediated nicotine metabolism. Biomarkers of nicotine metabolism and smoking exposure, including the ratio of trans-3-hydroxycotine to cotinine, a measure of P450 2A6 activity and plasma cotinine, or urinary total nicotine equivalents (the sum of nicotine and six metabolites) as measures of exposure are useful for addressing this challenge. However, to take full advantage of these biomarkers in the study of ethnic/racial differences in the risk of lung cancer requires the complete characterization of nicotine metabolism across ethnic/racial groups. Variation in metabolism pathways, other than those catalyzed by P450 2A6, can impact biomarkers of both nicotine metabolism and dose. This is clearly important for smokers with low levels of UGT2B10-catalyzed nicotine and cotinine glucuronidation because the UGT2B10 genotype influences plasma cotinine levels. Cotinine is not glucuronidated in 15% of African American smokers (compared to 1% of Whites) due to the prevalence of a UGT2B10 splice variant. This variant contributes significantly to the higher plasma cotinine levels per cigarette in this group and may also influence the accuracy of the 3HCOT to cotinine ratio as a measure of P450 2A6 activity.

Indexed as

BiomarkersCotinineCytochrome P-450 CYP2A6EthnicityGenetic VariationGlucuronosyltransferaseHumansLung NeoplasmsNicotineOxygenasesSmokingBiomarkersCotinineCYP2A6 protein, humanCytochrome P-450 CYP2A6dimethylaniline monooxygenase (N-oxide forming)GlucuronosyltransferaseNicotineOxygenasesUGT2B10 protein, human

Identifiers

PMID28092945
PMCPMC8205229
OpenAlexW2550204629

What OpenQuestion holds

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LicenceTDM
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.