Chris Wallace is accepting applications for PhD students.
- Cambridge Institute for Medical Research:
- Wellcome Trust Research Career Development Fellow, Head of the DIL statistics group.
I am a statistician working with biological datasets to understand the mechanisms underlying human disease and identify possible treatments. Such work is only possible with close collaboration with biologists, and I moved to the CIMR in 2009 to pursue these collaborations. During the GWAS era, we, and others, identified many genetic polymorphisms that alter risk of human diseases such as type 1 diabetes and hypertension. My focus has now mostly shifted towards identifying the molecular function of these variants. I am particularly interested in disentangling apparently colocalising traits, to understand if the effect of a variant on disease is mediated by its effect on another trait such as gene expression or whether a common variant alters risk of two related diseases, and to developing new and powerful methods for examining allelic expression imbalance within individuals. Statistically, my current work is focused on variable selection, Bayesian model averaging and mixture models.
genomics ; genetics ; allelic expression imbalance ; variable selection ; Bayesian model averaging ; mixture models
Wallace C. Statistical testing of shared genetic control for potentially related traits. Genet Epidemiol. 2013 Dec;37(8):802-13.
Pekalski ML, Ferreira RC, Coulson RM, Cutler AJ, Guo H, Smyth DJ, Downes K, Dendrou CA, Castro Dopico X, Esposito L, Coleman G, Stevens HE, Nutland S, Walker NM, Guy C, Dunger DB,Wallace C, Tree TI, Todd JA, Wicker LS. Postthymic expansion in human CD4 naive T cells defined by expression of functional high-affinity IL-2 receptors. J Immunol. 2013 Mar 15;190(6):2554-66.
Yang X, Todd JA, Clayton D, Wallace C. Extra-binomial variation approach for analysis of pooled DNA sequencing data. Bioinformatics. 2012 Nov 15;28(22):2898-904.
Wallace C, Rotival M, Cooper JD, Rice CM, Yang JH, McNeill M, Smyth DJ, Niblett D, Cambien F; Cardiogenics Consortium, Tiret L, Todd JA, Clayton DG, Blankenberg S. Statistical colocalization of monocyte gene expression and genetic risk variants for type 1 diabetes. Hum Mol Genet. 2012 Jun 15;21(12):2815-24.
Davison LJ, Wallace C, Cooper JD, Cope NF, Wilson NK, Smyth DJ, Howson JM, Saleh N, Al-Jeffery A, Angus KL, Stevens HE, Nutland S, Duley S, Coulson RM, Walker NM, Burren OS, Rice CM, Cambien F, Zeller T, Munzel T, Lackner K, Blankenberg S; Cardiogenics Consortium, Fraser P, Gottgens B, Todd JA, Attwood T, Belz S, Braund P, Cambien F, Cooper J, Crisp-Hihn A, Diemert P, Deloukas P, Foad N, Erdmann J, Goodall AH, Gracey J, Gray E, Gwilliams R, Heimerl S, Hengstenberg C, Jolley J, Krishnan U, Lloyd-Jones H, Lugauer I, Lundmark P, Maouche S, Moore JS, Muir D, Murray E, Nelson CP, Neudert J, Niblett D, O'Leary K, Ouwehand WH, Pollard H, Rankin A, Rice CM, Sager H, Samani NJ, Sambrook J, Schmitz G, Scholz M, Schroeder L, Schunkert H, Syvannen AC, Tennstedt S, Wallace C. Long-range DNA looping and gene expression analyses identify DEXI as an autoimmune disease candidate gene. Hum Mol Genet. 2012 Jan 15;21(2):322-33.
Wallace C, Smyth DJ, Maisuria-Armer M, Walker NM, Todd JA, Clayton DG. The imprinted DLK1-MEG3 gene region on chromosome 14q32.2 alters susceptibility to type 1 diabetes. Nat Genet. 2010 Jan;42(1):68-71.
Heinig M, Petretto E, Wallace C, Bottolo L, Rotival M, Lu H, Li Y, Sarwar R, Langley SR, Bauerfeind A, Hummel O, Lee YA, Paskas S, Rintisch C, Saar K, Cooper J, Buchan R, Gray EE, Cyster JG, Consortium C, Erdmann J, Hengstenberg C, Maouche S, Ouwehand WH, Rice CM, Samani NJ, Schunkert H, Goodall AH, Schulz H, Roider HG, Vingron M, Blankenberg S, Münzel T, Zeller T, Szymczak S, Ziegler A, Tiret L, Smyth DJ, Pravenec M, Aitman TJ, Cambien F, Clayton D, Todd JA, Hubner N, and Cook SA. A trans-acting locus regulates an anti-viral expression network and type 1 diabetes risk. Nature, 2010 467:460-464
Downes K, Pekalski M, Angus KL, Hardy M, Nutland S, Smyth DJ, Walker NM, Wallace C, and Todd JA. Reduced expression of IFIH1 is protective for type 1 diabetes. PLoS One, 2010 5.