Professor Aitman is Consultant Physician in the Imperial Academic Health Sciences Centre, Hammersmith Campus, holds a chair in Clinical and Molecular Genetics at the Imperial College London and is Head of the Section of Molecular Genetics and Rheumatology. He is Strategic Theme Leader for Genetics in the Imperial College Faculty of Medicine and chairs the Imperial Molecular Pathology Group, which he co-founded with others at Imperial in 2008. Imperial Molecular Pathology won substantial funds from the National Institute of Health Research (NIHR) to equip and refurbish a Laboratory for Molecular Pathology Research, which opened in January 2011. Professor Aitman is a Fellow of the Royal College of Physicians and Academy of Medical Sciences, and is a member of several external advisory boards including the Sir Jules Thorn Medical Advisory Committee and the editorial boards of Mammalian Genome, Physiological Genomics and BMC Bioinformatics. He was the Specialist Adviser for the House of Lords Science and Technology Committee’s Inquiry into Genomic Medicine (web link given below), and is currently a member of the Human Genetics Commission, the Government's advisory body on developments in Genetics.
Professor Aitman’s research has combined the use of classical genetics with genome technologies to investigate the genetics of common complex human disorders. These include the common syndromes of insulin resistance that predispose to diabetes and heart disease, and autoimmune diseases such as systemic lupus. The combined use of linkage analysis and microarray-based expression profiling led to identification of Cd36 as an insulin resistance gene in rats and humans and to defining the genetic control points for thousands of genes across the genome in a rodent model of the metabolic syndrome. More recently, genetic studies of autoimmune glomerulonephritis showed that a new type of genomic sequence variation, gene copy number variation, is a cause of autoimmune glomerulonephritis in rats and in the common human disease, systemic lupus erythematosus. These studies illustrate ways in which use of genome technologies can give insights into the molecular basis of common diseases, and have potential for translation to advancing the diagnosis, prevention and treatment of these disorders.
Professor Aitman is also Group Head of the Physiological Genomics and Medicine Group in the MRC Clinical Sciences Centre, where further details of his MRC research group, including his Group’s scientific publications, can be found.
Web link for House of Lords Genomic Medicine Report: http://www.publications.parliament.uk/pa/ld200809/ldselect/ldsctech/107/107i.pdf
et al., 2005, Integrated transcriptional profiling and linkage analysis for identification of genes underlying disease, Nature Genetics, Vol:37, ISSN:1061-4036, Pages:243-253
et al., 2013, Genomic pathology of SLE-associated copy-number variation at the FCGR2C/FCGR3B/FCGR2B locus., American Journal of Human Genetics, Vol:92, ISSN:0002-9297, Pages:28-40
et al., 2012, Complete cardiac regeneration in a mouse model of myocardial infarction, Aging-Us, Vol:4, ISSN:1945-4589, Pages:966-977
et al., 2012, Single nucleotide analysis of cytosine methylation by whole-genome shotgun bisulfite sequencing., Curr Protoc Mol Biol, Vol:Chapter 21
et al., 2012, Genetic basis of transcriptome differences between the founder strains of the rat HXB/BXH recombinant inbred panel, Genome Biology, Vol:13, ISSN:1474-760X
et al., 2011, FCGR3B copy number variation is associated with systemic lupus erythematosus risk in Afro-Caribbeans, Rheumatology, Vol:50, ISSN:1462-0324, Pages:1206-1210
et al., 2010, The genome sequence of the spontaneously hypertensive rat: Analysis and functional significance, Genome Research, Vol:20, ISSN:1088-9051, Pages:791-803
Fanciulli M, Petretto E, Aitman TJ, 2010, Gene copy number variation and common human disease, Clinical Genetics, Vol:77, ISSN:0009-9163, Pages:201-213
et al., 2008, Integrated genomic approaches implicate osteoglycin (Ogn) in the regulation of left ventricular mass, Nature Genetics, Vol:40, ISSN:1061-4036, Pages:546-552
et al., 2008, Jund is a determinant of macrophage activation and is associated with glomerulonephritis susceptibility, Nature Genetics, Vol:40, ISSN:1061-4036, Pages:553-559
et al., 2007, FCGR3B copy number variation is associated with susceptibility to systemic, but not organ-specific, autoimmunity, Nature Genetics, Vol:39, ISSN:1061-4036, Pages:721-723
et al., 2006, Copy number polymorphism in Fcgr3 predisposes to glomerulonephritis in rats and humans, Nature, Vol:439, ISSN:0028-0836, Pages:851-855