Dr Jeffrey Barrett
Jeffrey analyzes genomic variation in thousands of individuals to identify genetic risk factors for complex human diseases, especially those involving autoimmunity and infection.
Jeffrey Barrett became interested in human disease genetics during an undergraduate research project in Mark Daly's lab at the Whitehead Institute while he was a student at the Massachusetts Institute of Technology (MIT).
After he graduated in 2002 (BS, Physics) Jeff joined Mark's group full-time, where he developed software tools, including the widely used Haploview program, and analysed large scale human genetic variation datasets, including the HapMap project. In 2005 Jeff moved to Lon Cardon's group at the University of Oxford to undertake a DPhil in Statistics (jointly supervised by Peter Donnelly). While at Oxford Jeff worked on the design and subsequent analysis of the first generation of Genome Wide Association Studies (GWAS). He was a member of the analysis team for the Wellcome Trust Case Control Consortium (WTCCC), which comprised seven disease collections of 2000 cases each, with a shared set of 3000 controls. In addition to his work with the project as a whole, Jeff led the analysis of the replication effort in Crohn's disease (the most common type of inflammatory bowel disease [IBD]). In late 2007 Jeff moved to a post-doctoral position in David Clayton's group at the University of Cambridge, where he worked on meta-analyses and follow-up of GWAS in both Crohn's disease and type 1 diabetes, each of which resulted in the identification of twenty novel associations.
Jeff moved to the Wellcome Trust Sanger Institute in November 2008 to start a team in medical genomics, where he is continuing to work on both the general methodology for complex trait gene hunting and the specific follow-up projects of inflammatory diseases like IBD and infectious diseases like tuberculosis. Jeff is also excited to take advantage of the unique capabilities of the Sanger Institute, including genome-wide sequence and transcription datasets. He is involved in a number of international consortia, including the International IBD Genetics Consortium, the UK10K and Deciphering Developmental Disorders.
Selected Publications
-
Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease.
Nature 2012;491;7422;119-24
PUBMED: 23128233; PMC: 3491803; DOI: 10.1038/nature11582
-
Misuse of hierarchical linear models overstates the significance of a reported association between OXTR and prosociality.
Proceedings of the National Academy of Sciences of the United States of America 2012;109;18;E1048
PUBMED: 22499788; PMC: 3344973; DOI: 10.1073/pnas.1202539109
-
From HLA association to function.
Nature genetics 2012;44;3;235-6
PUBMED: 22366857; DOI: 10.1038/ng.2207
-
A systematic survey of loss-of-function variants in human protein-coding genes.
Science (New York, N.Y.) 2012;335;6070;823-8
PUBMED: 22344438; PMC: 3299548; DOI: 10.1126/science.1215040
-
Dense genotyping identifies and localizes multiple common and rare variant association signals in celiac disease.
Nature genetics 2011;43;12;1193-201
PUBMED: 22057235; PMC: 3242065; DOI: 10.1038/ng.998
-
Genetic risk prediction in complex disease.
Human molecular genetics 2011;20;R2;R182-8
PUBMED: 21873261; PMC: 3179379; DOI: 10.1093/hmg/ddr378
-
Imputation of low-frequency variants using the HapMap3 benefits from large, diverse reference sets.
European journal of human genetics : EJHG 2011;19;6;662-6
PUBMED: 21364697; PMC: 3110048; DOI: 10.1038/ejhg.2011.10
-
Synthetic associations are unlikely to account for many common disease genome-wide association signals.
PLoS biology 2011;9;1;e1000580
PUBMED: 21267062; PMC: 3022527; DOI: 10.1371/journal.pbio.1000580
-
Genome-wide meta-analysis increases to 71 the number of confirmed Crohn's disease susceptibility loci.
Nature genetics 2010;42;12;1118-25
PUBMED: 21102463; PMC: 3299551; DOI: 10.1038/ng.717
-
Evoker: a visualization tool for genotype intensity data.
Bioinformatics (Oxford, England) 2010;26;14;1786-7
PUBMED: 20507892; PMC: 3073232; DOI: 10.1093/bioinformatics/btq280
-
Genome-wide association study of ulcerative colitis identifies three new susceptibility loci, including the HNF4A region.
Nature genetics 2009;41;12;1330-4
PUBMED: 19915572; PMC: 2812019; DOI: 10.1038/ng.483
-
Genome-wide association study and meta-analysis find that over 40 loci affect risk of type 1 diabetes.
Nature genetics 2009;41;6;703-7
PUBMED: 19430480; PMC: 2889014; DOI: 10.1038/ng.381
-
Genome-wide association defines more than 30 distinct susceptibility loci for Crohn's disease.
Nature genetics 2008;40;8;955-62
PUBMED: 18587394; PMC: 2574810; DOI: 10.1038/ng.175
-
Sequence variants in the autophagy gene IRGM and multiple other replicating loci contribute to Crohn's disease susceptibility.
Nature genetics 2007;39;7;830-2
PUBMED: 17554261; PMC: 2628541; DOI: 10.1038/ng2061
-
Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls.
Nature 2007;447;7145;661-78
PUBMED: 17554300; PMC: 2719288; DOI: 10.1038/nature05911
-
Evaluating coverage of genome-wide association studies.
Nature genetics 2006;38;6;659-62
PUBMED: 16715099; DOI: 10.1038/ng1801
-
A haplotype map of the human genome.
Nature 2005;437;7063;1299-320
PUBMED: 16255080; PMC: 1880871; DOI: 10.1038/nature04226
-
Haploview: analysis and visualization of LD and haplotype maps.
Bioinformatics (Oxford, England) 2005;21;2;263-5
PUBMED: 15297300; DOI: 10.1093/bioinformatics/bth457


