Progressive pulmonary fibrosis may represent a precancerous condition. Indeed, the relative lung cancer (LC) risk is 3 to 7fold higher in Interstitial Lung Diseases (ILD), characterized by extensive fibrosis, than in patients without. Idiopathic pulmonary Fibrosis (IPF) per se has been recently proposed as a precancerous condition fulfilling the five criteria set by the National Cancer Institute. Myofibroblasts are the major player in pulmonary fibrosis: their proliferation and activation lead to an aberrant extracellular matrix (ECM) deposition that may progressively cause stiffness of the lung parenchyma further compromising local biochemical properties. Furthermore, cancer-associated fibroblasts (CAF) are also key components of the tumor microenvironment that contribute to the biology of the tumor, both favoring the spread of neoplastic cells and the resistance to therapy.
Lung fibroblasts, as well as CAF, represent a heterogeneous cell population originating from a variety of sources. Some authors have previously shown that a particular subset of fibroblasts acquires an invasive phenotype, which is essential for progressive fibrosis and possibly for carcinogenesis together with the surrounding pathological microenvironment onset.
Shedding new light on the similarities/differences between fibroblasts driving fibrosis in ILD and CAF could be helpful to identify specific markers and/or molecular pathways involved in carcinogenesis thus providing new therapeutic targets.
The recent advent of omic approaches, such as genome profiling or single-cell transcriptomic studies, will be of help to define the potentially common transition from normal lung fibroblasts to ILD-fibrotic ones and CAF. Novel models of in vitro cultures (i.e spheroids, organoids) might further provide suggestions on the mechanisms regulating myofibroblasts/alveolar cross-talking in fibrosis or pre-cancerous conditions.
Within this Research Topic, we aim to collect Original Research, Review, Mini-review, or Perspective articles reviewing and discussing the state and/or proposing novel insight in basic and translational research linking lung fibrosis and cancer progression.
Area of interest will include but not be limited to:
- Definition of common and alternative potential mesenchymal origin of ILD-fibroblasts and CAF;
- Exploration of biomarkers and therapeutic targets related to ILD-myofibroblasts and CAF;
- Microenvironment and ECM role in driving fibroblasts differentiation;
- Novel in vitro culture models (spheroid, organoid, bio-printed 3D models, organ-on-a-chip) to assess cell-to-cell relationships and the efficacy of new treatments;
- Correlations between aging and lung cancer inflammation.
Please note: manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent clinical or patient cohort, or biological validation in vitro or in vivo, which are not based on public databases) are not suitable for publication in this journal.
Progressive pulmonary fibrosis may represent a precancerous condition. Indeed, the relative lung cancer (LC) risk is 3 to 7fold higher in Interstitial Lung Diseases (ILD), characterized by extensive fibrosis, than in patients without. Idiopathic pulmonary Fibrosis (IPF) per se has been recently proposed as a precancerous condition fulfilling the five criteria set by the National Cancer Institute. Myofibroblasts are the major player in pulmonary fibrosis: their proliferation and activation lead to an aberrant extracellular matrix (ECM) deposition that may progressively cause stiffness of the lung parenchyma further compromising local biochemical properties. Furthermore, cancer-associated fibroblasts (CAF) are also key components of the tumor microenvironment that contribute to the biology of the tumor, both favoring the spread of neoplastic cells and the resistance to therapy.
Lung fibroblasts, as well as CAF, represent a heterogeneous cell population originating from a variety of sources. Some authors have previously shown that a particular subset of fibroblasts acquires an invasive phenotype, which is essential for progressive fibrosis and possibly for carcinogenesis together with the surrounding pathological microenvironment onset.
Shedding new light on the similarities/differences between fibroblasts driving fibrosis in ILD and CAF could be helpful to identify specific markers and/or molecular pathways involved in carcinogenesis thus providing new therapeutic targets.
The recent advent of omic approaches, such as genome profiling or single-cell transcriptomic studies, will be of help to define the potentially common transition from normal lung fibroblasts to ILD-fibrotic ones and CAF. Novel models of in vitro cultures (i.e spheroids, organoids) might further provide suggestions on the mechanisms regulating myofibroblasts/alveolar cross-talking in fibrosis or pre-cancerous conditions.
Within this Research Topic, we aim to collect Original Research, Review, Mini-review, or Perspective articles reviewing and discussing the state and/or proposing novel insight in basic and translational research linking lung fibrosis and cancer progression.
Area of interest will include but not be limited to:
- Definition of common and alternative potential mesenchymal origin of ILD-fibroblasts and CAF;
- Exploration of biomarkers and therapeutic targets related to ILD-myofibroblasts and CAF;
- Microenvironment and ECM role in driving fibroblasts differentiation;
- Novel in vitro culture models (spheroid, organoid, bio-printed 3D models, organ-on-a-chip) to assess cell-to-cell relationships and the efficacy of new treatments;
- Correlations between aging and lung cancer inflammation.
Please note: manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent clinical or patient cohort, or biological validation in vitro or in vivo, which are not based on public databases) are not suitable for publication in this journal.
