Evidence map›Paper›PMID 23908592›Full record

ArticleNeoplasia (New York, N.Y.)2013

Silica-induced chronic inflammation promotes lung carcinogenesis in the context of an immunosuppressive microenvironment.

Javier Freire, Daniel Ajona, Gabriel de Biurrun, Jackeline Agorreta, Victor Segura, Elizabeth Guruceaga, Anne-Marie Bleau, Ruben Pio, David Blanco, Luis M Montuenga

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Interleukin-1 signaling and CD4Frontiers in immunology · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. A rare case of silicosis with hepatitis B infection.Annals of medicine and surgery (2012) · 2022
    Article
  12. Review
  13. Review
  14. Pulmonary Inflammation and KRAS Mutation in Lung Cancer.Advances in experimental medicine and biology · 2021
    Article
  15. Article
  16. Review
  17. Article
  18. Silicosis and lung cancer: current perspectives.Lung Cancer (Auckland, N.Z.) · 2018
    Review
  19. Review
  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

10 authors at 2 institutions in 2 countries.

Javier FreireCenter for Applied Medical Research (CIMA), Pamplona, Spain.
Daniel Ajona
Gabriel de Biurrun
Jackeline Agorreta
Victor Segura
Elizabeth Guruceaga
Anne-Marie Bleau
Ruben Pio
David Blanco
Luis M Montuenga
Chartered Institute of Management Accountants · GBUniversidad de Navarra · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The association between inflammation and lung tumor development has been clearly demonstrated. However, little is known concerning the molecular events preceding the development of lung cancer. In this study, we characterize a chemically induced lung cancer mouse model in which lung cancer developed in the presence of silicotic chronic inflammation. Silica-induced lung inflammation increased the incidence and multiplicity of lung cancer in mice treated with N-nitrosodimethylamine, a carcinogen found in tobacco smoke. Histologic and molecular analysis revealed that concomitant chronic inflammation contributed to lung tumorigenesis through induction of preneoplastic changes in lung epithelial cells. In addition, silica-mediated inflammation generated an immunosuppressive microenvironment in which we observed increased expression of programmed cell death protein 1 (PD-1), transforming growth factor-β1, monocyte chemotactic protein 1 (MCP-1), lymphocyte-activation gene 3 (LAG3), and forkhead box P3 (FOXP3), as well as the presence of regulatory T cells. Finally, the K-RAS mutational profile of the tumors changed from Q61R to G12D mutations in the inflammatory milieu. In summary, we describe some of the early molecular changes associated to lung carcinogenesis in a chronic inflammatory microenvironment and provide novel information concerning the mechanisms underlying the formation and the fate of preneoplastic lesions in the silicotic lung.

Indexed as

AMP-Activated Protein KinasesAnimalsCell Transformation, NeoplasticCellular MicroenvironmentChronic DiseaseCytokinesDimethylnitrosamineFemaleImmunohistochemistryLungLung NeoplasmsMiceMice, Inbred BALB CMutationOligonucleotide Array Sequence AnalysisPneumoniaAMP-Activated Protein KinasesCytokinesDimethylnitrosamineHras protein, mouseProtein Serine-Threonine KinasesProto-Oncogene Proteins p21(ras)Silicon DioxideStk11 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID23908592
PMCPMC3730043
OpenAlexW1595518436

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.