Evidence map›Paper›PMID 33932402›Full record

ReviewThe Journal of biological chemistry

Biochemistry of nicotine metabolism and its relevance to lung cancer.

Sharon E Murphy

Open access · goldAbstract readReview
In one paragraph

Review in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
6.3field-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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. E‑Cigarettes Generate Gas Phase Ions.Environment & health (Washington, D.C.) · 2026
    Article
  6. Article
  7. Observational
  8. Article
  9. Article
  10. Article
  11. Article
  12. The Role of Single Nucleotide Polymorphisms at the Arg399Gln Locus of theInternational journal of molecular sciences · 2025
    Article
  13. Review
  14. Adverse Effects of Nicotine on Human Sperm Nuclear Proteins.The world journal of men's health · 2025
    Review
  15. Article
  16. Tobacco Biomarkers by Latino Heritage and Race, US, 2007 to 2014 National Health and Nutrition Examination Survey.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2024
    Article
  17. Review
  18. Methoxsalen Inhibits the Acquisition of Nicotine Self-Administration: Attenuation by Cotinine Replacement in Male Rats.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2024
    Article
  19. Association of Urinary Biomarkers of Tobacco Exposure with Lung Cancer Risk in African American and White Cigarette Smokers in the Southern Community Cohort Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2024
    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 MurphyMasonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA. Electronic address: murph062@umn.edu.
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 key addictive constituent of tobacco. It is not a carcinogen, but it drives smoking and the continued exposure to the many carcinogens present in tobacco. The investigation into nicotine biotransformation has been ongoing for more than 60 years. The dominant pathway of nicotine metabolism in humans is the formation of cotinine, which occurs in two steps. The first step is cytochrome P450 (P450, CYP) 2A6-catalyzed 5'-oxidation to an iminium ion, and the second step is oxidation of the iminium ion to cotinine. The half-life of nicotine is longer in individuals with low P450 2A6 activity, and smokers with low activity often decrease either the intensity of their smoking or the number of cigarettes they use compared with those with "normal" activity. The effect of P450 2A6 activity on smoking may influence one's tobacco-related disease risk. This review provides an overview of nicotine metabolism and a summary of the use of nicotine metabolite biomarkers to define smoking dose. Some more recent findings, for example, the identification of uridine 5'-diphosphoglucuronosyltransferase 2B10 as the catalyst of nicotine N-glucuronidation, are discussed. We also describe epidemiology studies that establish the contribution of nicotine metabolism and CYP2A6 genotype to lung cancer risk, particularly with respect to specific racial/ethnic groups, such as those with Japanese, African, or European ancestry. We conclude that a model of nicotine metabolism and smoking dose could be combined with other lung cancer risk variables to more accurately identify former smokers at the highest risk of lung cancer and to intervene accordingly.

Indexed as

Biomarkers, TumorCytochrome P-450 CYP2A6Half-LifeHumansLung NeoplasmsNicotineSmokingBiomarkers, TumorCYP2A6 protein, humanCytochrome P-450 CYP2A6NicotinecancercotinineCYP2A6cytochrome P450lung cancermetabolismnicotinesmokinguridine 5′-diphospho-glucuronosyltransferase (UDP-glucuronosyltransferase)

Identifiers

PMID33932402
PMCPMC8167289
OpenAlexW3159673490

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.