Evidence map›Paper›PMID 21098042›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2011

Interleukin 6, but not T helper 2 cytokines, promotes lung carcinogenesis.

Cesar E Ochoa, Seyedeh Golsar Mirabolfathinejad, Venado Ana Ruiz, Scott E Evans, Mihai Gagea, Christopher M Evans, Burton F Dickey, Seyed Javad Moghaddam

Open access · bronzeAbstract read
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Interleukin-6 -634C/G polymorphism is associated with lung cancer risk: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  2. Plants (Basel, Switzerland) · 2025
    Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. The Role of Respiratory Microbiota in Lung Cancer.International journal of biological sciences · 2021
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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

8 authors at 2 institutions in 2 countries.

Cesar E OchoaDepartment of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 1100, Houston, TX 77030, USA.
Seyedeh Golsar Mirabolfathinejad
Venado Ana Ruiz
Scott E Evans
Mihai Gagea
Christopher M Evans
Burton F Dickey
Seyed Javad Moghaddam
The University of Texas MD Anderson Cancer Center · USTecnológico de Monterrey · MX

Funding

Modeling Airway Lung Cancer and the Role of InflammationU01CA105352 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DEMAYO, FRANCESCO JOHN · 2004 to 2008
$4.2M
NCI NIH HHS U01 CA105352NCI NIH HHS UO1 CA105352
6 · The paper itself

Abstract

Several epidemiologic studies have found that smokers with chronic obstructive pulmonary disease (COPD), an inflammatory disease of the lung, have an increased risk of lung cancer compared with smokers without COPD. We have shown a causal role for COPD-like airway inflammation in lung cancer promotion in the CCSP(Cre)/LSL-K-ras(G12D) mouse model (CC-LR). In contrast, existing epidemiologic data do not suggest any definite association between allergic airway inflammation and lung cancer. To test this, CC-LR mice were sensitized to ovalbumin (OVA) and then challenged with an OVA aerosol weekly for 8 weeks. This resulted in eosinophilic lung inflammation associated with increased levels of T helper 2 cytokines and mucous metaplasia of airway epithelium, similar to what is seen in asthmatic patients. However, this type of inflammation did not result in a significant difference in lung surface tumor number (49 ± 9 in OVA vs. 52 ± 5 in control) in contrast to a 3.2-fold increase with COPD-like inflammation. Gene expression analysis of nontypeable Haemophilus influenzae (NTHi)-treated lungs showed upregulation of a different profile of inflammatory genes, including interleukin 6 (IL-6), compared with OVA-treated lungs. Therefore, to determine the causal role of cytokines that mediate COPD-like inflammation in lung carcinogenesis, we genetically ablated IL-6 in CC-LR mice. This not only inhibited intrinsic lung cancer development (1.7-fold) but also inhibited the promoting effect of extrinsic COPD-like airway inflammation (2.6-fold). We conclude that there is a clear specificity for the nature of inflammation in lung cancer promotion, and IL-6 has an essential role in lung cancer promotion.

Indexed as

Disease Models, AnimalAerosolsAnimalsBiomarkers, TumorCytokinesFemaleGene Expression ProfilingHaemophilus InfectionsHaemophilus influenzaeImmunoenzyme TechniquesIntegrasesInterleukin-6Lung NeoplasmsMiceMice, Inbred C57BLMice, KnockoutAerosolsBiomarkers, TumorCytokinesHras protein, mouseIntegrasesInterleukin-6OvalbuminProto-Oncogene Proteins p21(ras)RNA, MessengerScgb1a1 protein, mouseUteroglobin

Identifiers

PMID21098042
PMCPMC3058282
OpenAlexW2136932786

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.