Evidence map›Paper›PMID 26399408›Full record

ArticleBMC medicine2015

Idiopathic pulmonary fibrosis and cancer: do they really look similar?

Carlo Vancheri

Open access · goldAbstract read
In one paragraph

Article in BMC medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 5 pooled it
6.7field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 5 syntheses or guidelines pooled it, 90 citations in OpenAlex.

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  10. CD45+/ Col I+ Fibrocytes: Major source of collagen in the fibrotic lung, but not in passaged fibroblast cultures.Matrix biology : journal of the International Society for Matrix Biology · 2025
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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

1 author at 1 institution in 1 country.

Carlo VancheriRegional Centre for Interstitial and Rare Lung Diseases, Department of Clinical and Experimental Medicine, University of Catania, Via S. Sofia 78 - building 4, first floor, 95123, Catania, Italy. vancheri@unict.it.
University of Catania · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe aim of this opinion article is to understand to what extent idiopathic pulmonary fibrosis (IPF) can be considered, in its clinical and pathogenic features, similar to cancer. Indeed, IPF has common risk factors with cancer, a low survival, and, most importantly, epigenetic and genetic alterations, abnormal expression of microRNAs, cellular and molecular aberrances, and the activation of similar signalling pathways. DISCUSSION: The pathogenic link between the two diseases may have a number of practical consequences. It may improve our understanding of IPF drawing on cancer biology knowledge. In addition, the recognition of similar pathogenic pathways may also encourage the use of cancer drugs for the treatment of IPF. Nintedanib, an inhibitor of tyrosine kinase receptors initially developed for cancer, has been recently approved for the treatment of IPF thanks to the observation that these receptors are also abnormally activated in IPF. The vision of IPF as a cancer-like disease may improve our understanding of the pathogenesis of this disease also opening new scenarios for repositioning cancer drugs for IPF. In addition, it may increase the level of awareness towards this dreadful disease at the public, political, and healthcare level.

Indexed as

HumansIdiopathic Pulmonary FibrosisNeoplasmsSignal Transduction

Identifiers

PMID26399408
PMCPMC4581087
OpenAlexW1943036343

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.