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Modeling Molecular Pathogenesis of Idiopathic Pulmonary Fibrosis-Associated Lung Cancer in Mice

ABSTRACT: Modeling Molecular Pathogenesis of Idiopathic Pulmonary Fibrosis-Associated Lung Cancer in Mice

PROVIDER: PRJNA929956 | ENA |

REPOSITORIES: ENA

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Modeling Molecular Pathogenesis of Idiopathic Pulmonary Fibrosis-Associated Lung Cancer in Mice

Project description:Idiopathic Pulmonary Fibrosis (IPF) is characterized by progressive, often fatal loss of lung function due to overactive collagen production and tissue scarring. IPF patients have a sevenfold-increased risk of developing lung cancer. The COVID-19 pandemic has increased the number of patients with lung diseases, and infection can worsen prognoses for those with chronic lung diseases and disease-associated cancer. Understanding the molecular pathogenesis of IPFassociated lung cancer is imperative for identifying diagnostic biomarkers and targeted therapies that will facilitate prevention of IPF and progression to lung cancer. To understand how IPF-associated fibroblast activation, matrix remodeling, epithelial-mesenchymal transition, and immune modulation influences lung cancer predisposition, we developed a mouse model to recapitulate the molecular pathogenesis of pulmonary fibrosis-associated lung cancer using the bleomycin and Lewis Lung Carcinoma models. We demonstrate that development of pulmonary fibrosis-associated lung cancer is likely linked to increased abundance of tumor-associated macrophages and a unique gene signature that supports an immune-suppressive microenvironment through secreted factors. Not surprisingly, pre-existing fibrosis provides a pre-metastatic niche and results in augmented tumor growth, and tumors associated with bleomycin-induced fibrosis are characterized by a dramatic loss of cytokeratin expression, indicative of epithelial-to-mesenchymal transition. Implications: This characterization of tumors associated with lung diseases provides new therapeutic targets that may aid in the development of treatment paradigms for lung cancer patients with pre-existing pulmonary diseases.

2023-06-20 | GSE224134 | GEO

Idiopathic pulmonary fibrosis (IPF)

Project description:Idiopathic pulmonary fibrosis (IPF)

| PRJNA802122 | ENA

RNAseq in Idiopathic Pulmonary Fibrosis

Project description:RNAseq in Idiopathic Pulmonary Fibrosis

| PRJNA476994 | ENA

RNAseq in Idiopathic Pulmonary Fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and highly lethal lung disease with unknown etiology and poor prognosis.

2019-05-29 | GSE116086 | GEO

A role for complement in idiopathic pulmonary fibrosis

Project description:The pathogenesis of idiopathic pulmonary fibrosis is multifactorial and characterized by progressive fibrosis and excessive accumulation of extracellular matrix in the interstitium of the lung, and driven by an imbalance between anti-fibrotic and pro-fibrotic factors leading to collagen deposition. In the present study we wanted to identify proteins involved in these processes, and performed high-resolution proteomic profiling of bronchoalveolar lavage (BAL) from IPF patients and controls. The proteomic analysis of BAL demonstrated that the complement system was highly differentially regulated in IPF patients as compared with controls.

2023-07-31 | PXD036638 | Pride

Global Gene Expression Profiles of Fibroblasts from the Lungs of Patients with Idiopathic Pulmonary Fibrosis: The Role of CCL8

Project description:Analysis of Idiopathic pulmonary fibrosis (IPF) at gene expression level. The hypothesis tested in the present study was that Epigenetic mechanisms are likely to be associated with pathogenesis in IPF. To determine the DNA methylation change, and their effects on gene expression, we compared microarray data of DNA methylation and RNA expression. Results provide that among the genes whose DNA methylation status and RNA expression were both significantly altered between IPF-rapid and normal controls. Total RNA obtained from Idiopathic pulmonary fibrosis samples.

2015-10-31 | E-GEOD-71351 | biostudies-arrayexpress

Molecular Signatures of Idiopathic Pulmonary Fibrosis

Project description:Molecular Signatures of Idiopathic Pulmonary Fibrosis

| PRJNA725233 | ENA

Transcription profiling of human myofibroblasts isolated from patients with idiopathic pulmonary fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF), a chronic progressive lung disease of unknown etiology, is characterized by the expansion of myofibroblasts and abnormal deposition of extracellular matrix in the lung parenchyma. To elucidate the molecular mechanisms that lead to IPF, we analyzed myofibroblasts established from patients with IPF by oligonucleotide microarrays. Gene expression profiles revealed a novel pathophysiologic function of myofibroblasts as a generator of reactive oxygen species, and a self-defense mechanism against oxidative stress of their own generating. Experiment Overall Design: We isolated two myofibroblast cell culture from patients with idiopathic pulmonary fibrosis. Embryonic pulmonary fibroblast was used for the reference.

2008-06-15 | E-GEOD-6804 | biostudies-arrayexpress

Serial Analysis of Gene Expression molecular signature for disease progression in Idiopathic Pulmonary Fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive fibrosing interstitial lung disease that is unresponsive to current therapy. While it carries a median survival of less than 3 years its rate of progression varies widely between patients. We hypothesized that studying the gene expression profiles of physiologically stable patients and those in which the disease progressed rapidly after the initial diagnosis would aid in the search for biomarkers and contribute to the understanding of disease pathogenesis. We generated 12 Idiopathic Pulmonary Fibrosis (IPF) lung parenchyma SAGE profiles. Initial cluster analysis including 8 other public available lung SAGE libraries verified that the IPF transcriptome is distinct from normal lung tissue and other lung diseases like COPD. In order to identify candidate markers of disease progression we segregated the IPF SAGE profiles in two groups based on clinical parameters regarding lung volume and lung function.

2009-04-07 | E-GEOD-11665 | biostudies-arrayexpress

Transcriptomic Profiling of Fibrosis-Specific Epithelial Cells in Idiopathic Pulmonary Fibrosis

Project description:We aimed at characterizing disease-specific differences by comparing the transcriptomes of epithelial cells (ECs) from idiopathic pulmonary fibrosis (IPF) and non-IPF sources

2020-06-18 | GSE151673 | GEO

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