Annabelle Lewis

Summary

Affiliation: University of Oxford
Country: UK

Publications

  1. ncbi Severe polyposis in Apc(1322T) mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5
    Annabelle Lewis
    Molecular and Population Genetics Laboratory, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX3 7BN, UK
    Gut 59:1680-6. 2010
  2. ncbi The C-terminus of Apc does not influence intestinal adenoma development or progression
    Annabelle Lewis
    Molecular and Population Genetics Laboratory, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK
    J Pathol 226:73-83. 2012
  3. ncbi A basal gradient of Wnt and stem-cell number influences regional tumour distribution in human and mouse intestinal tracts
    Simon J Leedham
    Molecular and Population Genetics, Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, OX3 7BN, UK
    Gut 62:83-93. 2013
  4. ncbi Hereditary mixed polyposis syndrome is caused by a 40-kb upstream duplication that leads to increased and ectopic expression of the BMP antagonist GREM1
    Emma Jaeger
    Molecular and Population Genetics Laboratory, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK
    Nat Genet 44:699-703. 2012
  5. ncbi FBXW7 mutations typically found in human cancers are distinct from null alleles and disrupt lung development
    Hayley Davis
    Molecular and Population Genetics Laboratory, Wellcome Trust Centre for Human Genetics, Oxford University, Roosevelt Drive, Oxford OX3 7BN, UK
    J Pathol 224:180-9. 2011

Collaborators

Detail Information

Publications5

  1. ncbi Severe polyposis in Apc(1322T) mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5
    Annabelle Lewis
    Molecular and Population Genetics Laboratory, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX3 7BN, UK
    Gut 59:1680-6. 2010
    ..1322T mice had more severe polyposis but, surprisingly, these tumours had lower levels of nuclear β-catenin than Min tumours. The consequences of these different β-catenin levels were investigated...
  2. ncbi The C-terminus of Apc does not influence intestinal adenoma development or progression
    Annabelle Lewis
    Molecular and Population Genetics Laboratory, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK
    J Pathol 226:73-83. 2012
    ..We conclude that the C-terminus of APC does not influence intestinal adenoma development or progression...
  3. ncbi A basal gradient of Wnt and stem-cell number influences regional tumour distribution in human and mouse intestinal tracts
    Simon J Leedham
    Molecular and Population Genetics, Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, OX3 7BN, UK
    Gut 62:83-93. 2013
    ..The authors assessed effects of pan-intestinal Wnt activation on tissue homeostasis, taking into account underlying physiological Wnt activity and stem-cell number in each region of the bowel...
  4. ncbi Hereditary mixed polyposis syndrome is caused by a 40-kb upstream duplication that leads to increased and ectopic expression of the BMP antagonist GREM1
    Emma Jaeger
    Molecular and Population Genetics Laboratory, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK
    Nat Genet 44:699-703. 2012
    ..Increased GREM1 expression is predicted to cause reduced bone morphogenetic protein (BMP) pathway activity, a mechanism that also underlies tumorigenesis in juvenile polyposis of the large bowel...
  5. ncbi FBXW7 mutations typically found in human cancers are distinct from null alleles and disrupt lung development
    Hayley Davis
    Molecular and Population Genetics Laboratory, Wellcome Trust Centre for Human Genetics, Oxford University, Roosevelt Drive, Oxford OX3 7BN, UK
    J Pathol 224:180-9. 2011
    ..Fbxw7(R482Q) alleles are not functionally equivalent to heterozygous or homozygous null alleles, and we propose that they are selected in tumourigenesis because they cause a selective or partial loss of FBXW7 function...