University Lecturer in Statistical Genomics
Tel: +44 (0) 1223 748661
Jo’s interest in human genetics developed following the publication of the human genome project in 2000. After completing her PhD studies at the University of Durham, she joined the JDRF/Wellcome Trust Diabetes and Inflammation Laboratory (DIL; Director Professor John Todd) at the University of Cambridge, and undertook evaluation of statistical methods [1,2] and analyses of genetic data [3-6], under the guidance of Prof. David Clayton. Her specific interest was to improve the understanding of the genetic basis of type 1 diabetes and other autoimmune diseases .
During her 11 years at the DIL (resulting in 60 publications), she dissected the statistical disease associations of the major histocompatibility region on chromosome 6p21, the primary genetic risk locus in type 1 diabetes, which involved development of statistical methods [8,9]. As a follow-up to this effort, she was a member of the Type 1 Diabetes Genetics Consortium, with whom she also explored gene*gene interaction effects in type 1 diabetes .
She joined the CEU in March 2012 as a statistical geneticist.
Jo’s current interested involve understanding the role of genetics in cardiovascular diseases and risk factors. with a particular focus on blood pressure, stroke and coronary artery disease. She also maintains an interest in statistical methods for genetic analyses . She has identified 15 genetic loci associated with CAD  and through exploration of rare variants identified over 30 blood pressure associated loci  and over 70 lipid loci .
Jo is a member of the steering and/or executive committee of the CHD Exome+ consortium, the International Consortium of Blood Pressure (ICBP) and the MEGASTROKE consortium. She is also a member of the International Stroke Genetics Consortium.
- Howson JMM, Barratt BJ, Todd JA, Cordell HJ. Comparison of population- and family-based methods for genetic association analysis in the presence of interacting loci. Genet Epidemiol. 2005; 29: 51-67.
- Cordell HJ, Howson JMM, Clayton DG. Linkage analysis of a derived glucose phenotype in the Genetic Analysis Workshop 13 simulated data using a variety of Haseman-Elston based regression methods. BMC Genet. 2003; 4 Suppl 1:S6.
- Ueda H, Howson JMM, Esposito L, Heward J, Snook H, Chamberlain G, Rainbow DB, Hunter KM, Smith AN, Di Genova G, Herr MH, Dahlman I, Payne F, Smyth D, Lowe C, Twells RC, Howlett S, Healy B, Nutland S, Rance HE, Everett V, Smink LJ, Lam AC, Cordell HJ, Walker NM, Bordin C, Hulme J, Motzo C, Cucca F, Hess JF, Metzker ML, Rogers J, Gregory S, Allahabadia A, Nithiyananthan R, Tuomilehto-Wolf E, Tuomilehto J, Bingley P, Gillespie KM, Undlien DE, Ronningen KS, Guja C, Ionescu-Tirgoviste C, Savage DA, Maxwell AP, Carson DJ, Patterson CC, Franklyn JA, Clayton DG, Peterson LB, Wicker LS, Todd JA, Gough SC. Association of the T-cell regulatory gene CTLA4 with susceptibility to autoimmune disease. Nature. 2003; 423: 506-1
- Smyth DJ, Howson JMM, Lowe CE, Walker NM, Lam AC, Nutland S, Hutchings J, Tuomilehto-Wolf E, Tuomilehto J, Guja C, Ionescu-Tirgoviste C, Undlien DE, Ronningen KS, Savage D, Dunger DB, Twells RC, McArdle WL, Strachan DP, Todd JA. “Assessing the validity of the association between the SUMO4 M55V variant and risk of type 1 diabetes.” Nat Genet. 2005; 37: 110-1.
- Howson JMM,Dunger DB, Nutland S, Stevens H, Wicker LS, Todd JA. “A type 1 diabetes subgroup with a female bias is characterized by failure in tolerance to thyroid peroxidase at an early age and a strong association with the CTLA-4 gene.” Diabetologia. 2007; 50: 741-746.
- Field SF*, Howson JMM*, Maier L*, Walker S, Walker N, Armour J, Clayton D, Todd JA. “Experimental aspects of copy number variant assays at CCL3L1” Nature Medicine. 2009; 15: 1115-7
- Simmonds MJ, Howson JMM, Heward JM, Cordell HJ, Foxall H, Carr-Smith J, Gibson SM, Walker N, Tomer Y, Franklyn JA, Todd JA, Gough SC. “Regression mapping of association between the human leukocyte antigen region and Graves disease.” Am J Hum Genet. 2005; 76: 157-63.
- Howson JMM*, Nejentsev S*, Walker NM, Field SF, Szeszko JS, Stevens H, Lauder P, Hardy M, Masters J, Hulme J, Smyth D, Bailey R, Cooper JD, Campbell D, Clayton DC, Todd JA. Localisation of type 1 diabetes susceptibility to the major histocompatibility complex class I genes, HLA-A and HLA-B. Nature. 2007; 450: 887-92
- Howson JMM, WalkerNM, Clayton D, Todd JA. “Confirmation of HLA class II independent type 1 diabetes associations in the Major Histocompatibility Complex including HLA-B and HLA-A” Diabetes, Obesity and Metabolism. 2009; 11: 31-45 (Suppl 1)
- Howson JMM, Cooper JD, Smyth DJ, Walker NM, Stevens H, Yang JHM, She J, Eisenbarth GS, Rewers M, Todd JA, Akolkar B, Concannon P, Erlich HA, Julier C, Morahan G, Nerup J, Nierras C, Pociot F, Rich SS, and the Type 1 Diabetes Genetics Consortium. Evidence of gene-gene interaction and age-at-diagnosis effects in type 1 diabetes. Diabetes. 2012; 61: 3012-7
- Staley JR, Jones EPA, Wood AM, Kaptoge SK, Howson JMM, “Comparison of modelling approaches to testing for genetic associations in prospective studies” Eur. J Hum. Genet. 2017 25:854-862
- Howson JMM, + 70 Authors, Saleheen D. “Fifteen new risk loci for coronary artery disease highlight arterial wall-specific mechanisms” Nat. Genet. 2017 49:1113-1119
- Surendran P, + 200 authors, Howson JMM§, Munroe PB§. “Large scale trans-ethnic meta-analyses identify novel rare and common variants associated with blood pressure and hypertension.” Nat. Genet. 2016 48:1151-1161
- Liu D, + N authors, Howson JMM*, Danesh J*, McCarthy MI*, Cowan C*, Abecasis G*, Deloukas P*, Musunuru K*, Willer CJ*, Kathiresan S*, “Biological and clinical insights from genomic analysis of plasma lipids in >300,000 individuals” Nature Genetics 2017 49:1758-1766
* authors contributed equally