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Prof David Abraham
UCL-Medical School
Royal Free Campus
Rowland Hill Street
London
Hampstead
NW3 2PF
Appointment
  • Professor of Cell and Molecular Biology
  • Inflammation
  • Div of Medicine
  • Faculty of Medical Sciences
Biography

David Abraham is a Professor of cell and molecular biology, head of the research department of Inflammation, and Director of the Centre for Rheumatology and Connective Tissue Diseases, where he is also responsible for defining fibrosis strategy. His major research interests include the molecular and cell biology of connective tissue diseases, tissue repair processes, the genetic and molecular mechanisms underlying tissue scarring and fibrosis, and the development and use of in vivo systems of human disease (transgenic and genetically modified conventional and conditional knock-outs) as pre-clinical models to study the pathogenesis and treatment of connective tissue diseases. He has managed collaborations and interactions with industrial partners, leading to the successful licensing and translation of several targets from validation into clinical trials (Endothelin, PDGF, TGFbeta and IL-6).

After gaining a PhD, he held a research fellowship at the Kennedy Institute for Rheumatology in London, before becoming a Medical Research Council Travelling Fellow at Berkeley and the Jackson Laboratory in the USA. He worked as a senior scientist in genetics and mammalian development at the Medical Research Council's National Institute for Medical Research and then moved to UCL in 1997 to lead the Rheumatology research at the Royal Free campus

Research Summary

Our research programme employs basic scientific, clinical and translational methodologies to address fundamental questions related to diseases pathogenesis, assessment and treatment of connective tissue disease, specifically focusing on the scleroderma spectrum. The laboratory research focuses on understanding basic disease mechanisms in connective tissue disease and fibrosis. This has potential impact far beyond SSc. Five major research areas have emerged: 1. Biomarkers for disease including autoantibody profiles 2. Novel pro-inflammatory and fibrotic mediators 3. The origins of fibroblasts and myofibroblast differentiation 4. Molecular genetics of disease sub-sets 5. Development and study of Pre-clinical models. We have a unique clinical resource consisting of patient sample banks comprising of an ever increasing number of new and serial serum and plasma samples across the disease spectrum. We also have a tissue and cell bank which contains OCT and paraffin embedded tissue samples (skin, lung, Kidney) and frozen paired fibroblast cell lines (from lesional and non-lesional sites), and control fibroblast lines. Our genetic studies are supported by a nucleic acid bank which houses genomic DNA and RNA from over 4,000 patients within the disease spectrum. Our candidate gene approach links to gene and protein expression profiling analysis using microarrays, SNP genechips and proteomics. We have also utilised and developed a number of pre-clinical models for scleroderma. These include both inflammatory and non-inflammatory driven animal models of connective tissue scarring and fibrosis affecting the skin, heart, lungs, muscle, and kidney. These pre-clinical models in addition to primary cultures of leukocyte populations and fibroblasts have proved invaluable for the assessment of anti-inflammatory, immuno-modulators and anti-fibrotic compounds prior to their use in clinical trials.

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