Steele, Andrew - University of Southampton

个人简介

Dr Andrew Steele obtained his PhD in molecular microbiology from the University of Hertfordshire in 2003. His first postdoctoral position was in the laboratories of Professor Gillian Tozer and Professor David Shima at Gray Cancer Institute and CR-UK Lincoln’s Inn Fields, where he was involved in a collaborative project on hypoxia and its effect on vascular branching in human bladder carcinoma. Dr Steele moved to the laboratory of Dr RG Wickremasinghe at UCL Cancer Institute in 2004 where he worked closely for 8 years with Professor Victor Hoffbrand, Dr Archie Prentice and Professor Amit Nathwani investigating chemotherapy resistant mechanisms in Chronic Lymphocytic Leukaemia (CLL). Dr Steele Still works closely with Dr Wickremasinghe and Professor Nathwani at UCL. Dr Steele moved to the University of Southampton in March 2011 to take up a lectureship position in the Cancer Sciences Unit, working closely with Professors Graham Packham, Freda Stevenson and Mark Cragg and Drs Jon Strefford, Francesco Forconi, Kathy Potter and Andrew Duncombe on the biology of B cell malignancy but particularly CLL biology. Dr Steele works closely with a number of collaborators including Professor Peter Lydyard (University of Westminster) and Professor David Oscier and Drs Helen McCarthy and Renata Walevska at the Royal Bournemouth Hospital. Dr Steele was promoted to Senior lecturer (Associate Lecturer) in March 2013 after establishing with Professor Oscier a Leukemia and Lymphoma Research (LLR) funded South Coast tissue biobank, which stores with consent, blood samples from patients with a lymphoproliferative malignancy. Dr Steele’s current research focuses on investigating the effect of B cell receptor signalling (BCR) and microenvironmental signals on CLL biology and identifying novel therapeutic strategies for the treatment of CLL patients who have become resistant to conventional therapy due to genetic lesions such as 17p, 11q, Notch and SF3B1. Dr Steele is an expert in cell signalling and particularly cell death and survival mechanisms such as apoptosis and autophagy.

研究领域

Chronic lymphocytic leukaemia (CLL) is currently the most prevalent leukaemia in the western world with a very heterogeneous clinical course. Unfortunately even with the significant advances over the last 10 years, CLL is still incurable with chemotherapy. Dr Steele’s group works closely with the clinical staff and patients at Southampton General Hospital and Royal Bournemouth Hospital who provide primary tissue (blood) samples for his research. Working with CLL has the advantage that you can directly evaluate the biology of the primary tumours from patient. On average greater than 90% of the peripheral blood mononuclear cells (PBMC) are CLL cells. This means that our findings may be translatable directly into patients. Our on-going work uses biochemical approaches to study signal transduction in CLL with the overall goal of providing insights into the biology of CLL. This will enabling the identification of novel drugs and strategies which can be used to induce more effective apoptotic killing of CLL cells than is possible using conventional chemotherapy alone. Our recent studies fall into three categories; to understand how activating the B cell receptor (BCR) impacts on the survival and proliferation of CLL cells how signals within the microenvironment of the lymph nodes and bone marrow protect CLL cells from apoptosis and modify signalling via the BCR to identify novel chemotherapeutic agents and therapeutic strategies for the treatment of CLL with chemotherapy refractory disease and with aggressive disease due to 17p (TP53), 11q (ATM), Notch and SF3B1 deletion or mutation

近期论文

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IL-10 production by CLL cells is enhanced in the anergic IGHV mutated subset and associates with reduced DNA methylation of the IL10 locus - Drennan, S., D'Avola, A., Gao, Y., Weigel, C., Chrysostomou, E., Steele, A.J., Zenz, T., Plass, C., Johnson, P.W., Williams, A.O., Packham, G., Stevenson, F.K., Oakes, C.C. and Forconi, F. Published:2017Publication:LeukemiaPage Range:1-9doi:10.1038/leu.2016.356PMID:27890932 The dual Syk/JAK inhibitor cerdulatinib antagonises B-cell receptor and microenvironmental signaling in chronic lymphocytic leukemia - Blunt, Matthew, Koehrer, S., Dobson, R., Larrayoz, M., Wilmore, S., Hayman, A., Parnell, J., Smith, L. D., Davies, A., Johnson, P. W., Conley, P. B., Pandey, A., Strefford, J. C., Stevenson, F. K., Packham, G., Forconi, F., Coffey, G. P., Burger, J. and Steele, Andrew Published:2016Publication:Clinical Cancer ResearchPage Range:1-25doi:10.1158/1078-0432.CCR-16-1662 PEITC-mediated inhibition of mRNA translation is associated with both inhibition of mTORC1 and increased eIF2alpha phosphorylation in established cell lines and primary human leukemia cells - Yeomans, Alison, Lemm, Elizabeth, Wilmore, Sarah, Cavell, Breeze, Valle-Argos, Beatriz, Krysov, Sergey, Hidalgo, Marina, Leonard, Elodie, Willis, Anne E., Forconi, Francesco, Stevenson, Freda, Steele, Andrew, Coldwell, Mark and Packham, Graham Published:2016Publication:OncotargetPage Range:1-13doi:10.18632/oncotarget.11655PMID:27579538 To BH3 profile or not to BH3 profile - Blunt, Matthew and Steele, Andrew Published:2016Publication:BloodVolume:127, (25)Page Range:3111-3112doi:10.1182/blood-2016-04-711762PMID:27340250