S D Turner

Summary

Affiliation: University of Cambridge
Country: UK

Publications

  1. ncbi Vav-promoter regulated oncogenic fusion protein NPM-ALK in transgenic mice causes B-cell lymphomas with hyperactive Jun kinase
    Suzanne D Turner
    Laboratory of Lymphocyte Signalling and Development, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge CB2 4AT, UK
    Oncogene 22:7750-61. 2003
  2. ncbi Fusion tyrosine kinase mediated signalling pathways in the transformation of haematopoietic cells
    S D Turner
    Department of Pathology, Division of Molecular Histopathology, University of Cambridge, Lab Block Level 3, Addenbrooke s Hospital, Cambridge, UK
    Leukemia 20:572-82. 2006
  3. ncbi CD2 promoter regulated nucleophosmin-anaplastic lymphoma kinase in transgenic mice causes B lymphoid malignancy
    Suzanne D Turner
    Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Babraham, Cambridge CB2 4AT, UK
    Anticancer Res 26:3275-9. 2006
  4. ncbi The NPM-ALK tyrosine kinase mimics TCR signalling pathways, inducing NFAT and AP-1 by RAS-dependent mechanisms
    Suzanne D Turner
    Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Addenbrooke s Hospital, Cambridge, UK
    Cell Signal 19:740-7. 2007
  5. ncbi Jailbreak: oncogene-induced senescence and its evasion
    Fiona K E McDuff
    Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Lab Block Level 3, Addenbrooke s Hospital, Cambridge, UK
    Cell Signal 23:6-13. 2011
  6. ncbi The lymphoma-associated fusion tyrosine kinase ITK-SYK requires pleckstrin homology domain-mediated membrane localization for activation and cellular transformation
    Sue Rigby
    Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Cambridge CB2 2QQ, United Kingdom
    J Biol Chem 284:26871-81. 2009
  7. ncbi What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?
    S D Turner
    Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB2 4AT, UK
    Leukemia 19:1128-34. 2005
  8. ncbi The E2 ubiquitin conjugase Rad6 is required for the ArgR/Mcm1 repression of ARG1 transcription
    Suzanne D Turner
    Department of Biochemistry, University of Western Ontario, London, Canada N6A 5C1
    Mol Cell Biol 22:4011-9. 2002

Collaborators

Detail Information

Publications8

  1. ncbi Vav-promoter regulated oncogenic fusion protein NPM-ALK in transgenic mice causes B-cell lymphomas with hyperactive Jun kinase
    Suzanne D Turner
    Laboratory of Lymphocyte Signalling and Development, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge CB2 4AT, UK
    Oncogene 22:7750-61. 2003
    ..The new transgenic models provide a system for investigating the oncogenic events mediated by NPM-ALK in situ and a physiologically relevant context for developing tyrosine kinase inhibitor therapies of potential use in the clinic...
  2. ncbi Fusion tyrosine kinase mediated signalling pathways in the transformation of haematopoietic cells
    S D Turner
    Department of Pathology, Division of Molecular Histopathology, University of Cambridge, Lab Block Level 3, Addenbrooke s Hospital, Cambridge, UK
    Leukemia 20:572-82. 2006
    ..The FTK signalling field has matured to an exciting phase in which rapid advances are facilitating rational drug design...
  3. ncbi CD2 promoter regulated nucleophosmin-anaplastic lymphoma kinase in transgenic mice causes B lymphoid malignancy
    Suzanne D Turner
    Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Babraham, Cambridge CB2 4AT, UK
    Anticancer Res 26:3275-9. 2006
    ..Nucleophosmin-anaplastic lymphoma kinase expression is associated with a lymphoid malignancy, anaplastic large cell lymphoma, and is characterized by a t(2;5) chromosomal translocation...
  4. ncbi The NPM-ALK tyrosine kinase mimics TCR signalling pathways, inducing NFAT and AP-1 by RAS-dependent mechanisms
    Suzanne D Turner
    Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Addenbrooke s Hospital, Cambridge, UK
    Cell Signal 19:740-7. 2007
    ..Our results show that NPM-ALK mimics activated T-cell receptor signalling by inducing pathways associated with the activation of NFAT/AP-1 transcription factors that bind to promoter elements found in a broad array of cytokine genes...
  5. ncbi Jailbreak: oncogene-induced senescence and its evasion
    Fiona K E McDuff
    Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Lab Block Level 3, Addenbrooke s Hospital, Cambridge, UK
    Cell Signal 23:6-13. 2011
    ..We ask whether this is because rogue incipient cancer cells find ways to escape this imposed imprisonment or otherwise entirely avoid capture by senescence gate-keepers...
  6. ncbi The lymphoma-associated fusion tyrosine kinase ITK-SYK requires pleckstrin homology domain-mediated membrane localization for activation and cellular transformation
    Sue Rigby
    Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Cambridge CB2 2QQ, United Kingdom
    J Biol Chem 284:26871-81. 2009
    ....
  7. ncbi What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?
    S D Turner
    Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB2 4AT, UK
    Leukemia 19:1128-34. 2005
    ..This review focuses on recent advances in our understanding of the transforming signals induced by this fusion protein in mouse models...
  8. ncbi The E2 ubiquitin conjugase Rad6 is required for the ArgR/Mcm1 repression of ARG1 transcription
    Suzanne D Turner
    Department of Biochemistry, University of Western Ontario, London, Canada N6A 5C1
    Mol Cell Biol 22:4011-9. 2002
    ..In addition, analysis of an ada2 rad6 deletion strain indicated that the SAGA acetyltransferase complex and Rad6 act in the same pathway to repress ARG1 in rich medium...