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Open AccessReview

Idiopathic Pulmonary Fibrosis and Lung Cancer: Mechanisms and Molecular Targets

1,2,*,†, 2,3,4,† and 1,2,5
1
Department of Pharmacology, Faculty of Medicine, University of Valencia, 46010 Valencia, Spain
2
CIBERES, Health Institute Carlos III, 28029 Valencia, Spain
3
Pharmacy Unit, University Clinic Hospital of Valencia, 46010 Valencia, Spain
4
Institute of Health Research-INCLIVA, 46010 Valencia, Spain
5
Research and teaching Unit, University General Hospital Consortium, 46014 Valencia, Spain
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2019, 20(3), 593; https://doi.org/10.3390/ijms20030593
Received: 20 December 2018 / Revised: 18 January 2019 / Accepted: 28 January 2019 / Published: 30 January 2019
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PDF [1145 KB, uploaded 30 January 2019]
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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. View Full-Text
Keywords: idiopathic pulmonary fibrosis (IPF); lung cancer (LC); non-small cell lung cancer (NSCLC) idiopathic pulmonary fibrosis (IPF); lung cancer (LC); non-small cell lung cancer (NSCLC)
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Ballester, B.; Milara, J.; Cortijo, J. Idiopathic Pulmonary Fibrosis and Lung Cancer: Mechanisms and Molecular Targets. Int. J. Mol. Sci. 2019, 20, 593.

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