Evidence map›Paper›PMID 30704051›Full record

ReviewInternational journal of molecular sciences2019

Idiopathic Pulmonary Fibrosis and Lung Cancer: Mechanisms and Molecular Targets.

Beatriz Ballester, Javier Milara, Julio Cortijo

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed, 3 pooled it
24.1field-weighted citation impact, top 1% 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

183 citing papers in PubMed, 3 syntheses or guidelines pooled it, 307 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Folate metabolism-related gene signature reveals prognostic and immunological characteristics in idiopathic pulmonary fibrosis.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2026
    Article
  5. Postoperative acute exacerbations in patients with idiopathic pulmonary fibrosis undergoing lung cancer surgery.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2026
    Article
  6. Health effects of air pollution on chronic respiratory diseases.The Korean journal of internal medicine · 2026
    Review
  7. Article
  8. Review
  9. S100A4 Orchestrates Fibroblast Fate to Drive Fibrotic Remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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123 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

3 authors at 2 institutions in 1 country.

Beatriz BallesterDepartment of Pharmacology, Faculty of Medicine, University of Valencia, 46010 Valencia, Spain. beaballester7@gmail.com.
Javier MilaraCIBERES, Health Institute Carlos III, 28029 Valencia, Spain. xmilara@hotmail.com.
Julio CortijoDepartment of Pharmacology, Faculty of Medicine, University of Valencia, 46010 Valencia, Spain. julio.cortijo@uv.es.
Instituto de Salud Carlos III · ESHospital Clínico Universitario de Valencia · ES

Funding

Centro de Investigación Biomédica en Red Enfermedades Respiratorias CB06/06/0027Conselleria d'Educació, Investigació, Cultura i Esport 2017/023/UVConselleria d'Educació, Investigació, Cultura i Esport ACIF/2016/341Ministerio de Educación, Cultura y Deporte FIS PI17/02158Ministerio de Educación, Cultura y Deporte SAF2017-82913-RMinisterio de Educación, Cultura y Deporte TRA2009-0311
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is the most common idiopathic interstitial pulmonary disease with a median survival of 2⁻4 years after diagnosis. A significant number of IPF patients have risk factors, such as a history of smoking or concomitant emphysema, both of which can predispose the patient to lung cancer (LC) (mostly non-small cell lung cancer (NSCLC)). In fact, IPF itself increases the risk of LC development by 7% to 20%. In this regard, there are multiple common genetic, molecular, and cellular processes that connect lung fibrosis with LC, such as myofibroblast/mesenchymal transition, myofibroblast activation and uncontrolled proliferation, endoplasmic reticulum stress, alterations of growth factors expression, oxidative stress, and large genetic and epigenetic variations that can predispose the patient to develop IPF and LC. The current approved IPF therapies, pirfenidone and nintedanib, are also active in LC. In fact, nintedanib is approved as a second line treatment in NSCLC, and pirfenidone has shown anti-neoplastic effects in preclinical studies. In this review, we focus on the current knowledge on the mechanisms implicated in the development of LC in patients with IPF as well as in current IPF and LC-IPF candidate therapies based on novel molecular advances.

Indexed as

AnimalsAntineoplastic AgentsCarcinoma, Non-Small-Cell LungHumansIdiopathic Pulmonary FibrosisIndolesLung NeoplasmsMyofibroblastsPyridonesAntineoplastic AgentsIndolesnintedanibpirfenidonePyridonesidiopathic pulmonary fibrosis (IPF)lung cancer (LC)non-small cell lung cancer (NSCLC)

Identifiers

PMID30704051
PMCPMC6387034
OpenAlexW2913356394

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.