European IPF Network: Natural course, Pathomechani.. (eurIPFnet)
European IPF Network: Natural course, Pathomechanisms and Novel Treatment Options in Idiopathic Pulmonary Fibrosis
Start date: 01 Jan 2008,
End date: 30 Jun 2011
In the eurIPFnet consortium, leading European basic and clinical scientists in the field of interstitial lung diseases associate to jointly decipher the natural course and molecular pathomechanisms of Idiopathic Pulmonary Fibrosis (IPF) and to develop new therapeutic strategies for patients with IPF. This devastating disease affects about 360.000 patients in the EU and causes a substantial socioeconomic burden. IPF patients experience a gradual decrease in quality of life due to progressive dyspnoe and coughing, and usually die within 3-5 years upon diagnosis. There is currently no approved treatment available. Our translational research programme includes implementation of a European IPF registry (eurIPFreg), in which data with regard to natural course, familiar background and susceptibility factors of IPF will be collected, and of a European IPF biobank (eurIPFbank) of blood, bronchoalveolar lavage fluid, cells and tissue specimen of IPF. In these samples, we will perform transcriptome, proteome, phosphoproteome and lipidome analysis, cellular studies and genetic analysis to unravel the molecular pathways underlying IPF and to identify and establish new diagnostic and prognostic markers. Candidate gene verification will be performed in cell culture and animal studies, including siRNA and gene transfection technologies and development of genetically altered mice and will result in the development of new animal models of IPF. Identification of new therapeutic targets in these models will be followed by rapid commercial exploitation and early preclinical and early clinical evaluation. Ultimately, we wish to establish a unique, sustainable and internationally unrivalled European infrastructure for investigation and treatment of IPF. Our mission statement is straight-forward and clear: “Fighting for improved survival in Idiopathic Pulmonary Fibrosis”.
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