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Dr Suzanne Dawn Turner

Dr Suzanne Dawn Turner

Suzanne Turner is accepting applications for PhD students.

Suzanne Turner is available for consultancy.

Research Interests

Mechanisms of Lymphomagenesis.
Our research aims to dissect out the processes that lead from a healthy immune system to one which harbours a malignancy. We employ a paradigm of lymphomageneis in which a translocation breakpoint product called Nucelophosmin-Anaplastic Lymphoma Kinase (NPM-ALK) drives transformation of T-cells leading to a disease phenotype called Anaplastic Large Cell Lymphoma (ALCL). We are investigating the molecular mechanisms following expression of the NPM-ALK oncogene and presentation of ALCL using mouse models and tissue culture systems. NPM-ALK is a hyperactive tyrosine kinase which activates a plethora of downstream signal transduction pathways some of which are demonstrated in the figure. In addition to refining our knowledge of these pathways we are also investigating the contribution of antigenic stimulation to T-cell lymphomagenesis and its effects on the stability of the genome.


lymphoma ; animal models ; oncogenes


  • haematology
  • cancer

Key Publications

Ye X., Shokrollahi K., Rozen W.M., Whitaker I.S.,* and Turner S.D.* (2014) Anaplastic Large Cell Lymphoma (ALCL) and Breast Implants: Breaking down the evidence *joint corresponding authors. Mutation Research – Reviews, in press.

Turner S.D. (2013) Inimitable Imatinib: The range of targeted tumours expands to include T-cell malignancies. Leukemia 27(4):759.

Moti, N., Malcolm, T., Hamoudi, R., Mian, S., Garland, G., Hook, C.E., Burke, G.A.A., Wasik, M., Merkel, O., Lenner, L., Laurenti, E., Dick, J.E.and Turner, S.D. (2014) Anaplastic Large Cell Lymphoma stem cells possess a gene expression profile reflective of an early thymic progenitor pointing to a primitive cell of origin. Oncogene, In Press

McDuff, F.K.E., Lim, S-V., Dalbay, M. and Turner S.D. (2011) Assessment of the transforming potential of novel Anaplastic Lymphoma Kinase point mutants. Molecular Carcinogenesis doi: 10.1002/mc.21836
McDuff F.K.E., Hook C.E., Tooze R., Huntly B.J. Pandolfi P.P. and Turner S.D. (2011) Determining the Contribution of NPM1 heterozygosity to NPM-ALK-induced lymphomagenesis. Lab Investigation doi: 10.1038/labinvest.2011.96
McDuff F.K.E and Turner S.D. (2011) Aberrant Anaplastic Lymphoma Kinase Activity Induces a p53 and Rb-Dependent Senescence-Like Arrest in the Absence of Detectable p53 Stabilization. PLOS One 6(3): e17854. doi:10.1371/journal.pone.0017854

Other Publications

Marzec M., Halasa K., Liu X., Cheng M., Baldwin D., Tobias J.W., Schuster S., Woetmann A., Turner S.D., Odum N., and Wasik M.A. (2013)Malignant transformation of CD4+ T lymphocytes mediated by oncogenic kinase NPM/ALK recapitulates IL-2-induced cell signaling and gene expression reprogramming. Journal of Immunology 191(12):6200-7

Laimer, D., Dolznig, H., Kollmann, K., Vesely, P.W., Schlederer, M., Merkel, O., Schiefer, A., Hassler, M.R., Heider, S., Amenitsch, L., Thallinger, C., Staber, P.B., Simonitsch-Klupp, I., Artaker, M., Lagger, S., Turner, S.D., Pileri, S., Piccaluga, P.P., Valent, P., Messana, K., Landra, I., Weichhart, T., Knapp, S., Shehata, M., Todaro, M., Sexl, V., Höfler, G., Piva, R., Medico, E., Riggeri, B.A., Cheng, M., Eferl, R., Egger, G., Penninger, J.M., Jaeger, U., Moriggl, R., Inghirami, G.and Kenner, L. (2012)         Identification of PDGFR blockade as a rational and highly effective therapy for NPM-ALK driven lymphomas. Nature Medicine 18(11):1699-704
Zhang, Q., Wang, HY., Kantekure, K., Paterson, JC., Liu, X., Schaffer, A., Paulos, C, Milone, MC., Odum, N., Turner, SD., Marafioti, T., Wasik, MA. (2011) Oncogenic tyrosine kinase NPM-ALK induces expression of the growth-promoting receptor ICOS. Blood 118(11):3062-71.
Martinelli, P., Bonetti, P., Sironi, C., Pruneri, G., Fumagalli, C., Raviele, PR., Volorio, S., Pileri, S., Chiarle, R., Khoramian Tusi, B., McDuff, F.K.E., Turner, S.D., Inghirami, G., Pelicci, P.G. and Colombo, E. (2011) The lymphoma-associated NPM-ALK oncogene elicits a p16INKa/pRb-dependent tumour-suppressive pathway. Blood 117(24):6617-26.