Activation of oncogenic pathways in idiopathic pulmonary fibrosis

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9 Citations (Scopus)

Abstract

Idiopathic pulmonary fibrosis (IPF) is defined as a specific formof chronic, progressive fibrosing interstitial pneumonia of unknown cause. The most recent hypotheses on IPF pathogenesis suggest a central role of epithelial cell damage, followed by a dysregulated molecular cross talk between epithelial cells and fibroblasts. Thus, IPF progression has often been assimilated to that of cancer, and several signaling patterns appear to be disrupted in both diseases. Here,we analyze the expression in an IPF series of a panel of molecules, which are known to play a role in tumorigenic process. Our findings, although preliminary, reveal that IPF landscape is enriched in neoplastic potential expressed in a context of complex genomic polyclonality and cellular heterogeneity. These results provide a rationale for further investigations aimed to exploit—in a similar fashion to cancer—targeted therapies for a “precisionmedicine” approach to IPF.

Original languageEnglish
Pages (from-to)650-655
Number of pages6
JournalTranslational Oncology
Volume7
Issue number5
DOIs
Publication statusPublished - 2014

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Idiopathic Pulmonary Fibrosis
Epithelial Cells
Interstitial Lung Diseases
Fibroblasts
Neoplasms

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

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title = "Activation of oncogenic pathways in idiopathic pulmonary fibrosis",
abstract = "Idiopathic pulmonary fibrosis (IPF) is defined as a specific formof chronic, progressive fibrosing interstitial pneumonia of unknown cause. The most recent hypotheses on IPF pathogenesis suggest a central role of epithelial cell damage, followed by a dysregulated molecular cross talk between epithelial cells and fibroblasts. Thus, IPF progression has often been assimilated to that of cancer, and several signaling patterns appear to be disrupted in both diseases. Here,we analyze the expression in an IPF series of a panel of molecules, which are known to play a role in tumorigenic process. Our findings, although preliminary, reveal that IPF landscape is enriched in neoplastic potential expressed in a context of complex genomic polyclonality and cellular heterogeneity. These results provide a rationale for further investigations aimed to exploit—in a similar fashion to cancer—targeted therapies for a “precisionmedicine” approach to IPF.",
author = "Stella, {Giulia M.} and Simona Inghilleri and Ymera Pignochino and Michele Zorzetto and Tiberio Oggionni and Patrizia Morbini and Maurizio Luisetti",
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T1 - Activation of oncogenic pathways in idiopathic pulmonary fibrosis

AU - Stella, Giulia M.

AU - Inghilleri, Simona

AU - Pignochino, Ymera

AU - Zorzetto, Michele

AU - Oggionni, Tiberio

AU - Morbini, Patrizia

AU - Luisetti, Maurizio

PY - 2014

Y1 - 2014

N2 - Idiopathic pulmonary fibrosis (IPF) is defined as a specific formof chronic, progressive fibrosing interstitial pneumonia of unknown cause. The most recent hypotheses on IPF pathogenesis suggest a central role of epithelial cell damage, followed by a dysregulated molecular cross talk between epithelial cells and fibroblasts. Thus, IPF progression has often been assimilated to that of cancer, and several signaling patterns appear to be disrupted in both diseases. Here,we analyze the expression in an IPF series of a panel of molecules, which are known to play a role in tumorigenic process. Our findings, although preliminary, reveal that IPF landscape is enriched in neoplastic potential expressed in a context of complex genomic polyclonality and cellular heterogeneity. These results provide a rationale for further investigations aimed to exploit—in a similar fashion to cancer—targeted therapies for a “precisionmedicine” approach to IPF.

AB - Idiopathic pulmonary fibrosis (IPF) is defined as a specific formof chronic, progressive fibrosing interstitial pneumonia of unknown cause. The most recent hypotheses on IPF pathogenesis suggest a central role of epithelial cell damage, followed by a dysregulated molecular cross talk between epithelial cells and fibroblasts. Thus, IPF progression has often been assimilated to that of cancer, and several signaling patterns appear to be disrupted in both diseases. Here,we analyze the expression in an IPF series of a panel of molecules, which are known to play a role in tumorigenic process. Our findings, although preliminary, reveal that IPF landscape is enriched in neoplastic potential expressed in a context of complex genomic polyclonality and cellular heterogeneity. These results provide a rationale for further investigations aimed to exploit—in a similar fashion to cancer—targeted therapies for a “precisionmedicine” approach to IPF.

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