Evidence map›Paper›PMID 19890259›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2010

Common and unique biological pathways associated with smoking initiation/progression, nicotine dependence, and smoking cessation.

Ju Wang, Ming D Li

Abstract readComparative Study
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

52 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. CHRNA5-A3-B4, CYP2A6, and DBH Genetic Associations With Smoking Cessation Throughout Adulthood Within Two Longitudinal Studies of Women.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2025
    Article
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  8. An epidemiological introduction to human metabolomic investigations.Trends in endocrinology and metabolism: TEM · 2023
    Review
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  14. Observational
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  18. Examining sex differences in pleiotropic effects for depression and smoking using polygenic and gene-region aggregation techniques.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2019
    Article
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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

2 authors.

Ju WangSection of Neurobiology, Department of Psychiatry and Neurobehavioral Sciences, University of Virginia, Charlottesville, VA 22911, USA.
Ming D Li

Funding

MAPPING OF SUSCEPTIBILITY LOCI FOR NICOTINE DEPENDENCER01DA012844 · NIDA · UNIVERSITY OF VIRGINIA · PI LI, MING D · 1999 to 2013
$10.0M
GENE EXPRESSION PROFILING DURING EXPOSURE TO NICOTINER01DA013783 · NIDA · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI LI, MING D · 2000 to 2008
$3.9M
NIDA NIH HHS DA-12844NIDA NIH HHS DA-13783NIDA NIH HHS R01 DA012844NIDA NIH HHS R01 DA013783
6 · The paper itself

Abstract

Twin and family studies reveal a significant genetic contribution to the risk of smoking initiation and progression (SI/P), nicotine dependence (ND), and smoking cessation (SC). Further, numerous genes have been implicated in these smoking-related behaviors, especially for ND. However, no study has presented a comprehensive and systematic view of the genetic factors associated with these important smoking-related phenotypes. By reviewing the literature on these behaviors, we identified 16, 99, and 75 genes that have been associated with SI/P, ND, and SC, respectively. We then determined whether these genes were enriched in pathways important in the neuronal and brain functions underlying addiction. We identified 9, 21, and 13 pathways enriched in the genes associated with SI/P, ND, and SC, respectively. Among these pathways, four were common to all of the three phenotypes, that is, calcium signaling, cAMP-mediated signaling, dopamine receptor signaling, and G-protein-coupled receptor signaling. Further, we found that serotonin receptor signaling and tryptophan metabolism pathways were shared by SI/P and ND, tight junction signaling pathway was shared by SI/P and SC, and gap junction, neurotrophin/TRK signaling, synaptic long-term potentiation, and tyrosine metabolism were shared between ND and SC. Together, these findings show significant genetic overlap among these three related phenotypes. Although identification of susceptibility genes for smoking-related behaviors is still in an early stage, the approach used in this study has the potential to overcome the hurdles caused by factors such as genetic heterogeneity and small sample size, and thus should yield greater insights into the genetic mechanisms underlying these complex phenotypes.

Indexed as

Smoking CessationDatabases, GeneticDisease ProgressionGenetic Association StudiesGenetic Predisposition to DiseaseGenotypeHumansSignal TransductionSmokingTobacco Use Disorder

Identifiers

PMID19890259
PMCPMC2814000

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.