S D Turner

Summary

Affiliation: University of Cambridge
Country: UK

Publications

  1. ncbi request reprint 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. pmc Determining the contribution of NPM1 heterozygosity to NPM-ALK-induced lymphomagenesis
    Fiona K E Mduff
    Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Addenbrooke s Hospital, Cambridge, UK
    Lab Invest 91:1298-303. 2011
  3. pmc Aberrant anaplastic lymphoma kinase activity induces a p53 and Rb-dependent senescence-like arrest in the absence of detectable p53 stabilization
    Fiona Kate Elizabeth McDuff
    Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Cambridge, Cambridgeshire, United Kingdom
    PLoS ONE 6:e17854. 2011
  4. ncbi request reprint 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 request reprint 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
  6. ncbi request reprint 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
  7. doi request reprint 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
  8. ncbi request reprint 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
  9. pmc 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
  10. pmc 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

Publications10

  1. ncbi request reprint 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. pmc Determining the contribution of NPM1 heterozygosity to NPM-ALK-induced lymphomagenesis
    Fiona K E Mduff
    Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Addenbrooke s Hospital, Cambridge, UK
    Lab Invest 91:1298-303. 2011
    ..These data indicate that a tumor-suppressive role for NPM1 may depend on cellular and/or genetic context...
  3. pmc Aberrant anaplastic lymphoma kinase activity induces a p53 and Rb-dependent senescence-like arrest in the absence of detectable p53 stabilization
    Fiona Kate Elizabeth McDuff
    Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Cambridge, Cambridgeshire, United Kingdom
    PLoS ONE 6:e17854. 2011
    ..These data indicate that senescence may constitute an effective barrier to ALK-induced malignancies that ultimately must be overcome for tumor development...
  4. ncbi request reprint 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 request reprint 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...
  6. ncbi request reprint 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...
  7. doi request reprint 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...
  8. ncbi request reprint 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...
  9. pmc 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
    ....
  10. pmc 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...