Evidence map›Paper›PMID 19118942›Full record

ArticleCancer letters2009

Strain-dependent differences in susceptibility to lung cancer in inbred mice exposed to mainstream cigarette smoke.

Terry Gordon, Maarten Bosland

Open access · greenAbstract read
In one paragraph

Article in Cancer letters, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Phenotypic characteristics of commonly used inbred mouse strains.Journal of molecular medicine (Berlin, Germany) · 2020
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. E-cigarettes in patients with COPD: current perspectives.International journal of chronic obstructive pulmonary disease · 2017
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Lung carcinogenesis by tobacco smoke.International journal of cancer · 2012
    Review
  18. Article
  19. Antitumor activity of the investigational proteasome inhibitor MLN9708 in mouse models of B-cell and plasma cell malignancies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011
    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

2 authors.

Terry GordonDepartment of Environmental Medicine, NYU School of Medicine, 57 Old Forge Road, Tuxedo, NY 10987, USA. gordont@env.med.nyu.edu
Maarten Bosland

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ADRIANA HEGUY · 1985 to 2026
$83.1M
RESEARCH IN ENVIRONMENTAL HEALTH SCIENCES (CENTER GRANT)P30ES000260 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX · 1985 to 2020
$26.1M
NCI NIH HHS CA 016087NCI NIH HHS P30 CA016087NIEHS NIH HHS ES 0260NIEHS NIH HHS P30 ES000260
6 · The paper itself

Abstract

It is becoming increasingly clear that genetic susceptibility is an important host factor determining the effects of exposure to a number of airborne particles and gases. Although numerous studies have identified a genetic component for spontaneous pulmonary tumor development and for chemically induced lung cancer (e.g., urethane) in mice, a systematic examination of murine inter-strain differences in response to cigarette smoke inhalation has not been conducted. We addressed this research gap by examining the strain distribution pattern of lung cancer in nine inbred strains of mice exposed to 258 mg/m(3) mainstream cigarette smoke for 5 months followed by 4 months of rest. Lung tumors were enumerated on fixed lungs visualized at low magnification and on serial step sections examined microscopically. With the low magnification examination, we observed statistically significant increases in the number of lung tumors in cigarette smoke-exposed A/J and the genetically-related A/HeJ mice (p<0.05). While fewer tumors were identified by the microscopic enumeration method, it confirmed that significant increases in lung tumors occurred only in A/J and A/HeJ mice exposed to cigarette smoke (p<0.05). Thus, as predicted by epidemiologic studies and animal experiments using chemically induced lung cancer models, these findings suggest that genetic host factors play a significant role in the pulmonary tumorigenic response of mice to mainstream cigarette smoke.

Indexed as

Genetic Predisposition to DiseaseNicotianaSmokeAnimalsFemaleLung NeoplasmsMiceSpecies SpecificitySmoke

Identifiers

PMID19118942
PMCPMC2708971
OpenAlexW2013445570

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.