Evidence map›Paper›PMID 20525802›Full record

ReviewAmerican journal of respiratory cell and molecular biology2010

Lung injury and cancer: Mechanistic insights into ceramide and EGFR signaling under cigarette smoke.

Tzipora Goldkorn, Simone Filosto

Abstract readReview
In one paragraph

Review in American journal of respiratory cell and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Exosomes as Mediators of Chemical-Induced Toxicity.Current environmental health reports · 2019
    Review
  14. Modulators of Redox Metabolism in Head and Neck Cancer.Antioxidants & redox signaling · 2018
    Review
  15. Article
  16. Article
  17. Article
  18. Exosomes in Toxicology: Relevance to Chemical Exposure and Pathogenesis of Environmentally Linked Diseases.Toxicological sciences : an official journal of the Society of Toxicology · 2017
    Review
  19. Article
  20. Mitochondrial alterations during oxidative stress in chronic obstructive pulmonary disease.International journal of chronic obstructive pulmonary disease · 2017
    Review
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.

Tzipora GoldkornUniversity of California, Davis, 95616, USA. ttgoldkorn@ucdavis.edu
Simone Filosto

Funding

MOLECULAR CHARACTERIZATION OF A LUNG SPHINGOMYELINASER01HL066189 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI GOLDKORN, TZIPORA · 2001 to 2013
$2.7M
Proteasome-ErB1 Impaired Interaction in Lung HyperplasiaR01HL071871 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI GOLDKORN, TZIPORA · 2003 to 2006
$1.2M
NHLBI NIH HHS HL-66189NHLBI NIH HHS HL-71871
6 · The paper itself

Abstract

Cigarette smoke has been connected to an array of chronic lung diseases and is a major source of morbidity and mortality. Active smoking is responsible for approximately 90% of lung cancer cases. In addition, cigarette smoke is associated with other chronic pulmonary diseases such as pulmonary edema, chronic bronchitis, and pulmonary emphysema, the last two also termed chronic obstructive pulmonary disease (COPD). Lung cancer and COPD are developed very frequently in chronic cigarette smokers. It has been known for some time that lung cancer incidence increases in patients with COPD. Even the existence of some low-grade emphysema without noticeable airflow obstruction is associated with significantly elevated risk of lung cancer. These recent clinical insights demand new thinking and exploration of novel mechanistic studies to fully understand these observations. Lung injury and repair involve cell death and hyperplasia of airway epithelial cells and infiltration of inflammatory cells. All of these occur simultaneously. The mechanisms of cell death and hyperplasia in the lung constitute two sides of the coin of lung injury and repair. However, most molecular studies in airway epithelial cells center on the mechanism(s) of either cell growth and proliferation or cell death and the ceramide-generating machinery that drives aberrant induction of apoptotic cell death. Very few address both sides of the coin as an outcome of cigarette smoke exposure, which is the focus of this review.

Indexed as

AnimalsApoptosisCeramidesErbB ReceptorsHumansLung InjuryLung NeoplasmsOxidative StressSignal TransductionSmokingCeramidesEGFR protein, humanErbB Receptors

Identifiers

PMID20525802
PMCPMC2933544

What OpenQuestion holds

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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.