Dr Jane Owen-Lynch
Head of Division
Division of Biomedical and Life Sciences
Faculty of Health and Medicine
Tel: +44 1524 592330
Fax: +44 1524 593192
Current Research Interests
The major focus of my work is to determine the molecular mode of action of the abl oncogene. This oncogene is the causative agent in Chronic Myeloid Leukaemia and functions as a disregulated protein tyrosine kinase leading to abherrent survival of blood cell progenitors in the bone marrow. Activation of the Abl oncogene in cell line models of CML results in suppression of apoptosis, drug resistance, decreased adhesion to stromal cell layers, elevated levels of glucose transport and enhanced proliferative potential. Projects ongoing in this area include: -
- The role of certain signal transduction pathways e.g. protein kinase CbetaII and phosphatidylinositol-3-kinase and protein kinase B in mediating the anti-apoptotic and proliferative effects of Abl protein tyrosine kinase.
- Structure-function analysis using truncated forms of the Abl protein in order to determine the domains of the protein which are important in mediating its oncogenic effects.
The overall objective is to use the information gained from studies as described above to identify possible novel approaches for the treatment of leukaemia. In collaboration with the haematology department at Manchester and Lancaster hospitals studies will be continued using samples from patients with CML.
Another ongoing area of research concerns an investigation of the mechanisms of cortical development, i.e. how layering of neurones and glial cells is achieved, focusing on the role of specific cell types and signalling molecules linked to this process. The aim here is to discover how this process of normal development is disrupted in Hydrocephalus.
Cains S, Shepherd A, Nabiuni M, Owen-Lynch PJ, Miyan J. (2009) Addressing a folate imbalance in fetal cerebrospinal fluid can decrease the incidence of congenital hydrocephalus. J Neuropathol Exp Neurol. 68(4):404-16.
Owen-Lynch PJ (2008) Analyzing the oscillatory components of the dynamics of blood flow. J Appl Physiol. 105(1):374; author reply 389.
Robinson SJ, SŁnram-Lea SI, Leach J, Owen-Lynch PJ. (2008) The effects of exposure to an acute naturalistic stressor on working memory, state anxiety and salivary cortisol concentrations. Stress. 11(2):115-24.
Pierce A, Lu Y, Hamzah HG, Thompson S, Owen-Lynch PJ, Whetton AD, Spooncer E. (2006) Differential effect of leukaemogenic tyrosine kinases on cell motility is governed by subcellular localisation. Br J Haematol. 133(3):345-52.
Miyan JA, Zendah M, Mashayekhi F, Owen-Lynch PJ. (2006) Cerebrospinal fluid supports viability and proliferation of cortical cells in vitro, mirroring in vivo development. Cerebrospinal Fluid Res. 20;3:2.
Underhill-Day N, Pierce A, Thompson SE, Xenaki D, Whetton AD, Owen-Lynch PJ. (2006) Role of the C-terminal actin binding domain in BCR/ABL-mediated survival and drug resistance. Br J Haematol. 132(6):774-83.
Xenaki D, Pierce A, Underhill-Day N, Whetton AD, Owen-Lynch PJ. (2004) Bcr-Abl-mediated molecular mechanism for apoptotic suppression in multipotent haemopoietic cells: a role for PKCbetaII. Cell Signal. 16(2):145-56.
Bentley J, Itchayanan D, Barnes K, McIntosh E, Tang X, Downes CP, Holman GD, Whetton AD, Owen-Lynch PJ, Baldwin SA. (2003) Interleukin-3-mediated cell survival signals include phosphatidylinositol 3-kinase-dependent translocation of the glucose transporter GLUT1 to the cell surface. J Biol Chem. 278(41):39337-48.
Owen-Lynch PJ, Draper CE, Mashayekhi F, Bannister CM, Miyan JA. (2003) Defective cell cycle control underlies abnormal cortical development in the hydrocephalic Texas rat. Brain. 126(3):623-31.
Mashayekhi F, Draper CE, Bannister CM, Pourghasem M, Owen-Lynch PJ, Miyan JA. (2002) Deficient cortical development in the hydrocephalic Texas (H-Tx) rat: a role for CSF. Brain. 125(8):1859-74.
Bentley J, Walker I, McIntosh E, Whetton AD, Owen-Lynch PJ, Baldwin SA. (2001) Glucose transport regulation by p210 Bcr-Abl in a chronic myeloid leukaemia model. Br J Haematol. 112(1):212-5.
Pierce A, Spooncer E, Wooley S, Dive C, Francis JM, Miyan J, Owen-Lynch PJ, Dexter TM, Whetton AD. (2000) Bcr-Abl protein tyrosine kinase activity induces a loss of p53 protein that mediates a delay in myeloid differentiation. Oncogene. 2000 Nov 16;19(48):5487-97.
Tang X, Downes CP, Whetton AD, Owen-Lynch PJ. (2000) Role of phosphatidylinositol 3-kinase and specific protein kinase B isoforms in the suppression of apoptosis mediated by the Abelson protein-tyrosine kinase. J Biol Chem. 275(17):13142-8.