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Agency: Cordis | Branch: FP7 | Program: CP-FP | Phase: HEALTH-2007-2.4.3-8 | Award Amount: 3.83M | Year: 2008

CEED3 (Collaborative European Effort to Develop Diabetes Diagnostics) has as its central objective, the development of diagnostic tools to differentiate specific subgroups of diabetic patients to allow individualisation of patient care. CEED3 will achieve this by integrating basic science findings from animal models, cell studies, and large scale genetic studies with clinical observations and testing of patients phenotype. The development of diabetes diagnostic tools will involve a clearly defined process of discovery of potential novel genetic and non-genetic biomarkers, validation within test and population based data samples, development of a clinical application and then dissemination of this application. The areas of focus for the diabetes diagnostics will be three areas where there is potential for considerable improvement in care and reduction in the burden of diabetes: the identification of patients with specific subgroups of monogenic diabetes, the identification of non diabetic and diabetic subjects with initial pancreatic beta-cell dysfunction at high risk of rapidly deteriorating glycaemia and the detection of diabetic patients at increased risk of vascular complications. For each of these patient groups the identification of the subgroups will result in improved clinical care by allowing treatment to be tailored for the individual patient. Therefore, the goal of this proposal is to make a rapid translation from scientific discoveries to improved care for diabetic patients. CEED3 has assembled the best researchers, clinical samples and technical expertise in Europe to realise this goal.

Johns Hopkins University, The General Hospital Corporation and IntegraGen | Date: 2010-10-08

The invention provides methods featuring the use of polymorphisms in the JARID2 gene to diagnosis autism.

Agency: Cordis | Branch: FP7 | Program: CP-FP | Phase: HEALTH-2007-2.3.2-2 | Award Amount: 3.89M | Year: 2008

Improvements in TB control require the development of new tools for rapid and accurate diagnosis and intervention. This development is likely to benefit from more detailed knowledge of microbe-host relationships during infection. Following M. tuberculosis infection, only 5-10% of immunocompetent individuals develop TB. It is increasingly thought that the virulence of the infecting strain, together with host genetic factors, contribute to such differences between infected individuals. The M. tuberculosis W-Beijing lineage is one of the most successful mycobacterial families, in terms of morbidity and mortality. This lineage has been detected almost worldwide. The predominance of the W-Beijing lineage probably results from genetic advantages, including unidentified virulence factors and the induction/modification of specific host responses not yet thoroughly investigated. This project aims to unravel the links between differential host responses to M. tuberculosis infection and mycobacterial genetic diversity and virulence at the global genomic and post-genomic levels within the W-Beijing family, and between the W-Beijing family and other M. tuberculosis families, in order to improve our understanding of the epidemiological success of this particular lineage. Overall, this work will provide the scientific and clinical community with pioneering research and novel information increasing our understanding of the impact of M. tuberculosis strain diversity on virulence, immune response and pathology. This project will complement and expand the efforts of several internationally recognized laboratories to unveil new genotype-phenotype associations by integrating complex phenotypic data and information about mycobacterial genetic diversity.

The present invention discloses the identification of a human autism susceptibility gene, which can be used for the diagnosis, prevention and treatment of autism and related disorders, as well as for the screening of therapeutically active drugs. The invention more specifically discloses that the PRKCB 1 gene on chromosome 16 and certain alleles thereof are related to susceptibility to autism and represent novel targets for therapeutic intervention. The present invention relates to particular mutations in the PRKCBI gene and expression products, as well as to diagnostic tools and kits based on these mutations. The invention can be used in the diagnosis of predisposition to, detection, prevention and/or treatment of Asperger syndrome, pervasive developmental disorder, childhood disintegrative disorder, mental retardation, anxiety, depression, attention deficit hyperactivity disorders, speech delay or language impairment, epilepsy, metabolic disorder, immune disorder, bipolar disease and other psychiatric and neurological diseases.

The present invention relates to the technical field of hepatocellular carcinoma (HCC) management, and more precisely to the prognosis of HCC aggressiveness and associated therapeutic decisions. The invention provides a new prognosis method of HCC aggressiveness, based on determination in vitro and analysis of an expression profile comprising genes TAF9, RAMP3, HN1, KRT19, and RAN. The invention also provides kits for the prognosis of HCC aggressiveness, and methods of treatment of HCC in a subject based on a preliminary prognosis of said subject HCC aggressiveness.

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