Agency: Cordis | Branch: FP7 | Program: CP-FP | Phase: HEALTH.2012.1.4-1 | Award Amount: 8.01M | Year: 2013
In renal allograft recipients, 10-year graft survival has not improved over the past decades. Histological examination of graft biopsies has long been the gold standard to confirm graft injuries, but biopsies are invasive and histological grading is not very robust. There is thus a need for robust, non-invasive methods to predict and diagnose acute and chronic graft lesions, to improve patient treatment, quality of life and long-term graft survival. Also, there is an unmet need for better understanding of the immune and non-immune mechanisms of interstitial fibrosis /tubular atrophy and graft loss. Combining all the skills required to build upon previous findings, BIOMARGIN will offer such opportunities in renal transplantation by integrating several omics approaches (mRNA, miRNA, peptides, proteins, lipids and metabolites) in blood, graft tissue and urine, in a well thought out, multistage discovery-to-validation translational programme, following the highest European ethics and regulatory requirements, as well as quality controls and quality assessments at all clinical and analytical steps. It is probably one of the first programmes to pursue such an integrated and systematic research approach. BIOMARGIN aims to: (i) discover, select and validate blood and/or urine biomarkers of renal allograft lesions in adult and pediatric kidney transplant recipients; (ii) provide renal transplant physicians with non-invasive, robust diagnostic tests and interpretation algorithms enabling closer, more accurate, more predictive and/or less invasive monitoring of transplanted patients; (iii) help to avoid or diminish the use of biopsies and improve patient treatment, quality of life and long-term graft survival; (iv) help understand the mechanisms involved in the allograft injury processes which, combined with mass spectrometry imaging should offer pathologists new molecular targets and tools for renal graft biopsy analysis.
Agency: Cordis | Branch: FP7 | Program: MC-ITN | Phase: FP7-PEOPLE-ITN-2008 | Award Amount: 3.72M | Year: 2009
Aims: provide a cutting edge research training programme encompassing complementary approaches to the investigation of liver and pancreatic development and disease. Provide early stage researchers with a balanced mix of experience and skills in academic and industry based research. Give early stage researchers a set of transferrable skills which will improve their employment and career prospects. Objectives: 1) To provide a broad multi-disciplinary approach to liver and pancreatic development and disease which will ensure a solid foundation in research technology and methods. 2) To offer a number of multi-centre and cross-sector projects. 3) To organize regular meetings which will provide task-specific and complementary training in skills essential for career development. Implementation: 1) involvement of highly successful research leaders and groups (with expertise in different disciplines including systems biology and bioinformatics, developmental biology, genomics, genetics and epigenetics, cell biology, engineering and drug development) in design and running of this programme will ensure the cutting edge research methodology and multidisciplinary approach to training. 2) Each research project will involve minimum two partners. 3) Partners will alternate in organizing network meetings which will include laboratory courses, single-topic conferences and network workshops. 4) The experienced researchers recruited to the network will spend more time in the industrial setting and have more leadership training and responsibilities.
Agency: Cordis | Branch: H2020 | Program: RIA | Phase: PHC-14-2015 | Award Amount: 6.00M | Year: 2016
The goal of BATCure is to advance the development of new therapeutic options for a group of rare lysosomal diseases - neuronal ceroid lipofuscinoses (NCL) or Batten disease. There are > thousand affected across Europe, with a combined incidence of c.1:100 000. The NCLs are devastating and debilitating genetic disorders that mainly affect children, who suffer progressive dementia and motor decline, visual failure and epilepsy, leading to a long period of complete dependence on others, and eventually a premature death. Existing palliative treatment can reduce, but does not eliminate, the burden of seizures and the progressively worsening effects on the whole body due to decreasing CNS influence and control. There are no curative treatments in the clinic for any type of NCL. We will follow a novel integrated strategy to identify specific gene and small molecule treatments for three genetic types of Batten disease that include the most prevalent world-wide, juvenile CLN3 disease, and in southern and mediterranean Europe, CLN6 and CLN7 diseases. To develop new therapies for these 3 types of Batten disease, BATCure will: 1. Create new models, tools and technologies for developing and testing therapies 2. Further delineate disease biology and gene function to identify new therapeutic target pathways utilising yeast and pluripotent stem cell models 3. Identify biochemical therapeutic target pathways, facilitate effective evaluation of preclinical therapies and improve diagnostics 4. Extend a comprehensive natural history beyond the brain to include cardiology, the spinal cord, PNS, psychiatric and metabolic changes 5. Identify new and repurpose existing small molecule therapy 6. Triage new compound treatments in zebrafish, a high-throughput small vertebrate model 7. Deliver and monitor new treatments using mouse models 8. Provide a novel mechanism to involve patients and their families to inform and fully contribute to therapy development and prepare for clinical trials
Agency: Cordis | Branch: FP7 | Program: CP-IP | Phase: HEALTH.2013.2.1.1-1 | Award Amount: 16.16M | Year: 2013
Recently intense research identified around 4,000 single nucleotide polymorphisms (SNPs) associated with human age related diseases such as metabolic disorders. Despite their highly significant association to pathology, the functional role of these genetic variants is, in most cases, yet to be elucidated. The evolutionary distance of most animal models from humans represents a major limitation for the functional validation of these SNPs. To overcome these difficulties, HUMAN will generate mouse models carrying human hepatocytes or pancreatic cells from either primary cells (hepatocytes) or induced pluripotent stem cells (iPSCs). This innovative approach offers the unique possibility of studying function of genetic risk variants associated with metabolic diseases in an integrated living system (the mouse body), but within human-derived organs, i.e. liver and pancreas. iPSCs used to generate hepatocytes and cells will derive from extreme phenotypes, i.e. patients affected by severe metabolic diseases such as type 2 diabetes (T2D) or subjects selected for exceptional healthy longevity (subjects over 105 years and offspring of nonagenarian sibships) all fully clinically and metabolically characterised and genotyped; they will be selected according to the best combination of risk and protective alleles. We will test the effect of different nutritional regimes (e.g. high fat diet, caloric restriction), to disentangle the complex molecular mechanisms and circuitry across organs (e.g. hypothalamus-liver axis) which lead to pathology. HUMAN associates a core of outstanding basic research institutions to leading European biotech SMEs, and has the capability to produce at least 500 humanised mice. HUMAN will generate iPSCs biobanks and comprehensively manage all associated information. HUMAN is uniquely situated to drive innovation towards a better knowledge of the genetic basis of human metabolic diseases, thereby contributing to healthier aging of European citizens.