Agency: Cordis | Branch: FP7 | Program: MC-IAPP | Phase: PEOPLE-2007-3-1-IAPP | Award Amount: 1.66M | Year: 2008
SME RECEPTOR is a transfer of knowledge programme which will bring top scientists from industry and academia together to address key questions in nuclear receptor research. The programme of research, which is implemented through the two way exchange of researchers between three leading research organisations and three specialist innovative SMEs, will develop methodology to tackle one of the most pressing medical challenges in Europe characterization of the nuclear receptor role and the development of drugs targeting the complex symptoms characterized by the metabolic syndrome. SME RECEPTOR will exploit new opportunities for drug design provided by advances in bioinformatics and transgenic technology. This will enhance the understanding of basis mechanisms underlying nuclear receptor actions and their translation into the physiological regulation of diseases. Since cardiovascular toxicity is a major factor involved in both early and late drug failure, SME RECEPTOR will primarily focus on the development of early screening methods for cardiovascular toxicity, as well as to expand the knowledge of the governing molecular mechanisms. A key factor is the ability to translate the knowledge generated within this exchange programme into more advanced and efficient development of novel pharmaceuticals within the industry. The project will generate a group of scientists with unique knowledge and international expertise in nuclear receptor biology as well as nuclear receptor targeting pharmaceuticals. The mutually beneficial two way transfer of knowledge between industry and academia will provide a career boost to the researchers who will acquire leading new knowledge, complementary training and a detailed understanding of the research culture in their opposite sector. The project will further promote industry-academic networking, creating a strategic long-lasting industry-academia partnership.
Agency: Cordis | Branch: FP7 | Program: CP-FP | Phase: HEALTH.2010.2.4.1-6 | Award Amount: 4.23M | Year: 2011
Pancreatic cancer is one of the most lethal human cancers with a five-year survival rate of less than 5%. Late presentation and a high level of resistance to chemotherapeutic drugs are among the major reasons for this dismal prognosis. The presence of the highest degree of desmoplasia among all solid tumours and the fact that chronic inflammatory pancreatic disease is associated with an increased risk for pancreatic cancer indicate, that the tumour microenvironment is of particular importance for carcinogenesis in the pancreas. The long-term objective of this proposal is to increase survival of pancreatic cancer patients by exploring the contribution of the tumour microenvironment to the failure of presently available oncological treatments. For this purpose the clinical observation will be reverse-translated into innovative in-vitro and mouse models closely mimicking the human disease. This will allow a profound study of the mechanistic basis of treatment failure by deciphering the complex network between components of the microenvironment and cancer cells leading to increased resistance to chemotherapy and infiltrative growth along adjacent lymphatic and neural structures as well as metastatic spread. Identification of cancer (stem) cell-autonomous as well as stromal-derived mediators of invasion and chemoresistance will lead to novel drug targets to overcome the current therapeutic dilemma. The consortium has been specifically designed to include all required levels of expertise: 1) surgical and medical oncology groups conducting the largest clinical trials for pancreatic cancer in Europe, 2) expert pancreatic pathologists, 3) basic scientists focused on the study of carcinogenesis and tumour microenvironment interactions in the pancreas, 4) molecular oncology groups that have developed genetically engineered mouse models faithfully recapitulating human pancreatic cancer, as well as 5) pharmaceutical industry specialised on drug development.