Dr Annabelle Lewis
Wellcome Trust Centre for Human Genetics, Roosevelt Dr.
Genome wide association studies have been used to identify common sequence variants associated with increased colorectal cancer risk in the general population. I am currently working on characterising the functional, gene regulatory elements tagged by these variants and identifying the mechanism by which they predispose to cancer.
Previously in the Tomlinson lab, I have studied common mutations in the colorectal cancer tumour suppressor genes APC and FBXW7, to investigate the relationship between the type of mutation and disease severity.
Lewis, A., Freeman-Mills, L., de la Calle-Mustienes, E., Giraldez-Perez, R.M., Davis, H., Jaeger, E. et al. (2014). A Polymorphic Enhancer near GREM1 Influences Bowel Cancer Risk through Differential CDX2 and TCF7L2 Binding. Cell reports 8, 983-990.
Jaeger E, Leedham S, Lewis A, Segditsas S, Becker M, Cuadrado PR, et al., (2012) Hereditary mixed polyposis syndrome is caused by a 40-kb upstream duplication that leads to increased and ectopic expression of the BMP antagonist GREM1. Nat Genet 44(6): 699-703
Lewis A, Segditsas S, Deheragoda M, Pollard P, Jeffery R, Nye E et al., (2010) Severe polyposis in Apc(1322T) mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5. Gut 59(12): 1680-1686
Lewis A*, Green K*, Dawson C, Redrup L, Huynh KD, Lee JT, Hemberger M, Reik W(2006)Epigenetic dynamics of the Kcnq1 imprinted domain in the early embryo.Development 133(21): 4203-10
Lewis A*, Mitsuya K*, Umlauf D, Smith P, Dean W, Walter J, Higgins M, Feil R, Reik W (2004) Imprinting on distal chromosome 7 in the placenta involves repressive histone methylation independent of DNA methylation. Nat Genet 36(12): 1291-1295