S D Turner
Affiliation: University of Cambridge
- Vav-promoter regulated oncogenic fusion protein NPM-ALK in transgenic mice causes B-cell lymphomas with hyperactive Jun kinaseSuzanne 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...
- Fusion tyrosine kinase mediated signalling pathways in the transformation of haematopoietic cellsS 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...
- CD2 promoter regulated nucleophosmin-anaplastic lymphoma kinase in transgenic mice causes B lymphoid malignancySuzanne 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...
- The NPM-ALK tyrosine kinase mimics TCR signalling pathways, inducing NFAT and AP-1 by RAS-dependent mechanismsSuzanne 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...
- Jailbreak: oncogene-induced senescence and its evasionFiona 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...
- The lymphoma-associated fusion tyrosine kinase ITK-SYK requires pleckstrin homology domain-mediated membrane localization for activation and cellular transformationSue Rigby
Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Cambridge CB2 2QQ, United Kingdom
J Biol Chem 284:26871-81. 2009....
- 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...
- The E2 ubiquitin conjugase Rad6 is required for the ArgR/Mcm1 repression of ARG1 transcriptionSuzanne 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...