Evidence map›Paper›PMID 22280835›Full record

ArticleLife sciences2012

New associations of the genetic polymorphisms in nicotinic receptor genes with the risk of lung cancer.

Anna Chikova, Hans-Ulrich Bernard, Igor B Shchepotin, Sergei A Grando

Abstract read
In one paragraph

Article in Life sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Drug Discovery Targeting Nicotinic Acetylcholine Receptors for Hearing Loss.International journal of molecular sciences · 2026
    Review
  3. α9-Containing Nicotinic Receptors in Cancer.Frontiers in cellular neuroscience · 2021
    Review
  4. Review
  5. Article
  6. Article
  7. Examination of the Involvement of Cholinergic-Associated Genes in Nicotine Behaviors in European and African Americans.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2017
    Article
  8. TwoInternational journal of chronic obstructive pulmonary disease · 2017
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

4 authors at 3 institutions in 3 countries.

Anna ChikovaDepartment of Dermatology, University of California, Irvine, CA 92697, USA.
Hans-Ulrich Bernard
Igor B Shchepotin
Sergei A Grando
University of California, Irvine · USD.I. Ivanovsky Institute of Virology Russian Academy of Medical Sciences · RUNational Cancer Institute · UA

Funding

Epithelial Acetylcholine Oral Biology and PathologyR01DE014173 · NIDCR · UNIVERSITY OF CALIFORNIA-IRVINE · PI GRANDO, SERGEI A · 2002 to 2012
$3.1M
Nicotinic Receptor Ligands and Tobacco-induced Lung CancerR01ES017009 · NIEHS · UNIVERSITY OF CALIFORNIA-IRVINE · PI GRANDO, SERGEI A · 2010 to 2014
$1.7M
NIDCR NIH HHS DE14173NIDCR NIH HHS R01 DE014173NIEHS NIH HHS ES017009NIEHS NIH HHS R01 ES017009
6 · The paper itself

Abstract

aimsPrevious studies revealed association of lung cancer risk with single nucleotide polymorphisms (SNPs) in chromosome 15q25 region containing CHRNA5-CHRNA3-CHRNB4 nicotinic acetylcholine receptor (nAChR) subunit gene cluster. The genetic variations in other lung nAChRs remained unknown. In this study, we perform case-control analysis of CHRNA9 and CHRNA3 genes using 340 non-small cell lung cancer cases and 435 controls. MAIN

methodsAll exons, 3'UTR, intron 1 and parts of other introns surrounding exons 2-5 of CHRNA9 gene as well as exons 2, 3 of CHRNA3 gene and parts of surrounding intronic regions were sequenced. The study was controlled for gender, age and ethnicity related differences. Each SNP in analyzed groups was assessed by allele frequency, genotype distribution and haplotype analysis. KEY

findingsThe case-control analysis revealed that an increased risk is associated with two SNPs in CHRNA9, rs56159866 and rs6819385, and one in CHRNA3, rs8040868. The risk was reduced for three SNPs in CHRNA9, rs55998310, rs56291234, and newly discovered rs182073550, and also in carriers of the haplotype NP_060051.2 containing ancestral N442 variant of α9. SIGNIFICANCE: The nonsynonymous substitutions can produce receptors exhibiting unique ligand-binding and downstream signaling characteristics, synonymous as well all intronic SNPs may affect protein production at the transcriptional and/or translational levels, or just manifest association with cancer by genetic linkage to other alleles. Elucidation of the mechanisms by which individual genetic variations in α9 affect predisposition to lung cancer may lead to development of personalized approaches to cancer prevention and treatment as well as protection against tobacco consumption.

Indexed as

Polymorphism, Single NucleotideCarcinoma, Non-Small-Cell LungCase-Control StudiesGenetic Predisposition to DiseaseHaplotypesHumansLung NeoplasmsReceptors, NicotinicRisk FactorsReceptors, Nicotinic

Identifiers

PMID22280835
PMCPMC3341501
OpenAlexW2069445531

What OpenQuestion holds

Textmetadata
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.