Evidence map›Paper›PMID 18000061›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

Epithelial NF-kappaB activation promotes urethane-induced lung carcinogenesis.

Georgios T Stathopoulos, Taylor P Sherrill, Dong-Sheng Cheng, Robert M Scoggins, Wei Han, Vasiliy V Polosukhin, Linda Connelly, Fiona E Yull, Barbara Fingleton, Timothy S Blackwell

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

118 citing papers in PubMed, 1 synthesis or guideline pooled it, 187 citations in OpenAlex.

  1. Pooled it
  2. Circadian rhythms in health and disease.Molecular biomedicine · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Nuclear factor kappa B expression in non-small cell lung cancer.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

58 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

10 authors at 3 institutions in 1 country.

Georgios T StathopoulosDepartment of Medicine, Division of Allergy, Pulmonary, and Critical Care, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. gstathop@med.uoa.gr
Taylor P Sherrill
Dong-Sheng Cheng
Robert M Scoggins
Wei Han
Vasiliy V Polosukhin
Linda Connelly
Fiona E Yull
Barbara Fingleton
Timothy S Blackwell
Pulmonary and Allergy Associates · USVanderbilt University · USVA Tennessee Valley Healthcare System · US

Funding

Role of Eicosanoids In Modulating Endotoxin Induced LiveP01HL066196 · NHLBI · VANDERBILT UNIVERSITY · PI CHRISTMAN, BRIAN W · 2002 to 2006
$9.0M
MOLECULAR REGULATION OF LUNG INFLAMMATION BY NF-KBR01HL061419 · NHLBI · VANDERBILT UNIVERSITY · PI BLACKWELL, TIMOTHY S · 1999 to 2006
$1.5M
NHLBI NIH HHS HL61419NHLBI NIH HHS HL66196NHLBI NIH HHS P01 HL066196NHLBI NIH HHS R01 HL061419
6 · The paper itself

Abstract

Chronic inflammation is linked to carcinogenesis in several organ systems. In the lungs, NF-kappaB, a central effector of inflammatory responses, is frequently activated in non-small-cell lung cancer, but its role in tumor promotion has not been studied. Several lines of evidence indicate that ethyl carbamate (urethane)-induced lung tumor formation, a prototypical mouse model of multistage lung carcinogenesis, is potentiated by inflammation. We found that mouse strains susceptible to lung tumor formation (FVB, BALB/c) exhibited early NF-kappaB activation and inflammation in the lungs after urethane treatment. However, a resistant strain (C57B6) failed to activate NF-kappaB or induce lung inflammation. In FVB mice, we identified urethane-induced NF-kappaB activation in airway epithelium, as well as type II alveolar epithelial cells and macrophages. Using an inducible transgenic mouse model (FVB strain) to express a dominant inhibitor of NF-kappaB specifically in airway epithelial cells, we found that urethane-induced lung inflammation was blocked and tumor formation was reduced by >50%. Selective NF-kappaB inhibition resulted in increased apoptosis of airway epithelial cells at 2 weeks after urethane treatment in association with a marked reduction of Bcl-2 expression. These studies indicate that NF-kappaB signaling in airway epithelium is integral to tumorigenesis in the urethane model and identify the NF-kappaB pathway as a potential target for chemoprevention of lung cancer.

Indexed as

AnimalsCell Transformation, NeoplasticDisease SusceptibilityEpithelial CellsFemaleLung NeoplasmsMaleMiceNF-kappa BProto-Oncogene Proteins c-bcl-2UrethaneNF-kappa BProto-Oncogene Proteins c-bcl-2Urethane

Identifiers

PMID18000061
PMCPMC2141808
OpenAlexW2007470751

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.